Multi-trait Genome-Wide Analysis Identified 20 Novel Loci for Sarcopenia-Related Traits in UK Biobank.

This study aims to identify novel loci associated with sarcopenia-related traits in UK Biobank (UKB) through multi-trait genome-wide analysis. To identify novel loci associated with sarcopenia, we integrated the genome-wide association studies (GWAS) of usual walking pace (UWP) and hand grip strength (HGS) to conduct a joint association study known as multi-trait analysis of GWAS (MTAG). We performed a transcriptome-wide association study (TWAS) to analyze the results of MTAG in relation to mRNA expression data for genes identified in skeletal muscle.

Prediction on the changes in potential suitable areas for mangroves along the coast of Guangxi and the threat from invasion.

As one of the important blue carbon pools in tropical and subtropical intertidal zones, mangroves are widely distributed along the coast of Guangxi in China. To deeply explore the variations of potential suitable habitats for mangroves in China under the background of climate change, based on remote sensing interpretation data of coastal wetlands in Guangxi, global marine environment and bioclimatic environment data in 2021, we constructed a maximum entropy habitat distribution model to simulate the spatial distribution of potential suitable areas for mangroves and the invasive species, along the coast of Guangxi, and predicted the patterns under extreme climate change scenarios (SSP5-8.5).

Identification of LRRK2 gene related to sarcopenia and neuroticism using weighted gene co-expression network analysis.

Background: Sarcopenia is reported to be associated with neuroticism, but the mechanisms are not fully understood. Thus, it's of vital importance to elucidate the molecular mechanism of sarcopenia and neuroticism and to explore the potential molecular target of medical therapies for sarcopenia and neuroticism.

Methods: The expression datasets (sarcopenia: GSE111006 and neuroticism: GSE60491) were downloaded from the Gene Expression Omnibus.

Alpha-Asarone modulates kynurenine disposal in muscle and mediates resilience to stress-induced depression via PGC-1α induction.

Introduction: Kynurenine (KYN) accumulation in periphery induces brain injury, responsible for depression. α-Asarone is a simple phenylpropanoids that exerts beneficial effects on central nervous system. However, the effect of α-asarone on periphery is unexplored.

Muscone and (+)-Borneol Cooperatively Strengthen CREB Induction of Claudin 5 in IL-1-Induced Endothelium Injury.

Claudin 5 is one of the major proteins of tight junctions and is responsible for cerebrovascular integrity and BBB function. Muscone and (+)-borneol is the major ingredient of moschus and borneolum, respectively, with antioxidative and anti-inflammatory activities. This study investigated whether muscone and (+)-borneol combination protected claudin 5 by targeting ROS-mediated IL-1 accumulation.

Hydroxysafflor Yellow A Blocks HIF-1 Induction of NOX2 and Protects ZO-1 Protein in Cerebral Microvascular Endothelium.

Zonula occludens-1 (ZO-1) is a tight junction protein in the cerebrovascular endothelium, responsible for blood-brain barrier function. Hydroxysafflor yellow A (HSYA) is a major ingredient of safflower ( L.) with antioxidative activity.

The mitochondrial β-oxidation enzyme HADHA restrains hepatic glucagon response by promoting β-hydroxybutyrate production.

Disordered hepatic glucagon response contributes to hyperglycemia in diabetes. The regulators involved in glucagon response are less understood. This work aims to investigate the roles of mitochondrial β-oxidation enzyme HADHA and its downstream ketone bodies in hepatic glucagon response.

Tanshinone IIA prevents LPS-induced inflammatory responses in mice via inactivation of succinate dehydrogenase in macrophages.

Metabolic reprogramming is associated with NLRP3 inflammasome activation in activated macrophages, contributing to inflammatory responses. Tanshinone IIA (Tan-IIA) is a major constituent from Salvia miltiorrhiza Bunge, which exhibits anti-inflammatory activity. In this study, we investigated the effects of Tan-IIA on inflammation in macrophages in focus on its regulation of metabolism and redox state.

Whole-exome sequencing and genome-wide association studies identify novel sarcopenia risk genes in Han Chinese.

Sarcopenia is a complex polygenic disease, and its molecular mechanism is still unclear. Whole lean body mass (WLBM) is a heritable trait predicting sarcopenia. To identify genomic loci underlying, we performed a whole-exome sequencing (WES) of WLBM variation with high sequencing depth (more than 40*) in 101 Chinese subjects.

Livin Regulates H2A.X Phosphorylation and Promotes Autophagy in Colon Cancer Cells via a Novel Kinase Activity.

To investigate Livin-mediated regulation of H2A.X phosphorylation via a novel kinase activity and its effect on autophagy in colon cancer cells. The interaction between Livin and H2A.

Association between 1 Homozygous Deletion and Risk of Pancreatic Cancer: A Meta Analysis.

Objective To clarify the possible association of 1 homozygous deletion with the susceptibility to pancreatic cancer. Methods We searched PubMed database, Chinese Journal Full Text Database (CNKI), and EMBASE to find the eligible studies published up to April 18, 2018 for evaluating the relationship between 1 homozygous deletion and pancreatic cancer. The frequency of null genotype for 1 between the pancreatic cancer group and the healthy control group was compared with - test, and odds ratios (s) value and 95% confidence interval (95% ) were calculated.

Inactivation of NF-κB2 (p52) restrains hepatic glucagon response via preserving PDE4B induction.

Glucagon promotes hepatic gluconeogenesis and maintains whole-body glucose levels during fasting. The regulatory factors that are involved in fasting glucagon response are not well understood. Here we report a role of p52, a key activator of the noncanonical nuclear factor-kappaB signaling, in hepatic glucagon response.

Livin promotes colon cancer progression by regulation of H2A.X via JMJD6.

Livin is an important member of the human inhibitor of apoptosis proteins (IAPs) family. IAPs are proteins with antiapoptotic abilities, and their functions are different from the Bcl-2 (B-cell lymphoma-2) family proteins. However, the precise role of Livin in colon cancer progression remains unclear.

Restrains Reactive Oxygen Species-Associated Pulmonary Fibrosis via Targeting Nrf2-Nox4 Redox Balance.

Pulmonary fibrosis (PF) is characterized by myofibroblast activation, which can be triggered by oxidative stress. In this study, we investigated the antifibrotic effect of the ethyl acetate extract of (EASM) on PF and examined the underlying molecular mechanism. EASM suppressed myofibroblast activation with reduced extracellular matrix deposition in the lungs of mice subjected to bleomycin (BLM) challenge, demonstrating the inhibitory effects on PF.

American Ginseng and Asian Ginseng Intervention in Diet-Induced Obese Mice: Metabolomics Reveals Distinct Metabolic Profiles.

American ginseng and Asian ginseng, which occupy prominent positions in the list of best-selling natural products in the West and East, are suitable for different indications in the traditional pharmacological uses. Currently, the effects of American ginseng and Asian ginseng in the protection against metabolic dysfunction and the differences between them are still unknown. Herein, an untargeted metabolomics based on liquid chromatography-quadrupole time-of-flight mass spectrometry (LC-Q-TOF-MS) was determined.

A mitochondrion-targeting tanshinone IIA derivative attenuates myocardial hypoxia reoxygenation injury through a SDH-dependent antioxidant mechanism.

The medicinal values of many natural bioactive components to treat myocardial ischaemia reperfusion (I/R) injury are limited by their poor permeability. Herein, we demonstrate that an original tanshinone IIA derivative (Tan-TPP) could probably be improved myocardial I/R injury suppressant. It was optimised by mitochondria targeting group triphenylphosphine (TPP).

Tanshinone IIA Activates Nuclear Factor-Erythroid 2-Related Factor 2 to Restrain Pulmonary Fibrosis via Regulation of Redox Homeostasis and Glutaminolysis.

Aims: Pulmonary fibrosis (PF) is characterized by myofibroblast activation through oxidative stress. However, the precise regulation of myofibroblast transdifferentiation remains largely uncharacterized.

Results: In this study, we found that tanshinone IIA (Tan-IIA), an active component in the root of Salvia miltiorrhiza Bunge, can suppress reactive oxygen species (ROS)-mediated activation of myofibroblast and reduce extracellular matrix deposition in bleomycin (BLM)-challenged mice through the regulation of nuclear factor-erythroid 2-related factor 2 (Nrf2).

Compounds containing trace element copper or zinc exhibit as potent hyperuricemia inhibitors via xanthine oxidase inactivation.

Compounds containing trace elements copper or zinc are potential gout and hyperuricemia suppressant by virtue of their inhibiting effect on xanthine oxidase/xanthine dehydrogenase (XOD/XDH) and anti-inflammatory and anti-oxidative function. In this study, compounds Cu(hmy-paa)·SO·HO (simplified as CuHP) and Zn(hmy-paa)·SO·HO (simplified as ZnHP) are synthesized, where hmy-paa stands for 3-(4-hydroxy-3-methoxyphenyl)-N-(1H-pyrazol-3-yl)acrylamide). The ligand hmy-paa is composed of functional ferulic acid and 3-aminopyrazole.

Neotuberostemonine inhibits the differentiation of lung fibroblasts into myofibroblasts in mice by regulating HIF-1α signaling.

Pulmonary fibrosis may be partially the result of deregulated tissue repair in response to chronic hypoxia. In this study we explored the effects of hypoxia on lung fibroblasts and the effects of neotuberostemonine (NTS), a natural alkaloid isolated from Stemona tuberosa, on activation of fibroblasts in vitro and in vivo. PLFs (primary mouse lung fibroblasts) were activated and differentiated after exposure to 1% O or treatment with CoCl (100 μmol/L), evidenced by markedly increased protein or mRNA expression of HIF-1α, TGF-β, FGF2, α-SMA and Col-1α/3α, which was blocked after silencing HIF-1α, suggesting that the activation of fibroblasts was HIF-1α-dependent.