[Analysis of the Traits of Nitrogen Metabolism Pathways for Several Forest Soils in Eastern China].

Nitrogen metabolism pathways mediated by microorganisms play an important role in maintaining the structure and functional stability of soil ecosystems. Clarifying the relationships between microbial communities and nitrogen metabolism pathways can expand our understanding of nitrogen metabolism pathways at a microscopic level. However, the horizontal gene transfer of microorganisms means that taxonomy-based methods cannot be easily applied. A growing number of studies have shown that functional traits affect community construction and ecosystem functions. Using methods based on functional traits to study soil microbial communities can, therefore, better characterize nitrogen metabolism pathways. Here, five typical forest soils in China, namely black soil(Harbin, Heilongjiang), dark-brown earth(Changbaishan, Jilin), yellow-brown earth(Wuhan, Hubei), red earth(Fuzhou, Fujian), and humid-thermo ferralitic soil(Ledong, Hainan), were selected to study the traits of nitrogen metabolism pathways using metagenomic technology combined with the trait-based methods. The studied nitrogen metabolism pathways were ammonia assimilation, nitrate dissimilatory reduction, nitrate assimilatory reduction, denitrification, nitrification, nitrogen fixation, and anaerobic ammonia oxidation. The results showed that bacteria dominated the metagenomic library, accounting for 98.02% of all the sequences. Across all domains, the most common pathway was ammonia assimilation. For example, an average of 2830 ammonia assimilation pathway genes were detected for every million annotated bacterial sequences. In comparison, nitrogen fixation and anaerobic ammonia oxidation were the least detected pathways, accounting for 28.3 and 10.7 per million sequences, respectively. Different microorganisms can participate in a same nitrogen metabolism pathway, and the community structure of different soils was variable. The five typical forest soils in China show the same microbial nitrogen metabolism pathway traits; however, the community structure of the microorganisms mediating these processes was found to vary.

Quercetin attenuates high fructose feeding-induced atherosclerosis by suppressing inflammation and apoptosis via ROS-regulated PI3K/AKT signaling pathway.

Quercetin is a dietary flavonoid compound extracted from various plants, such as apple and onions. Previous studies have revealed its anti-inflammatory, anti-cancer, antioxidant and anti-apoptotic activities. This study investigated the ability of quercetin to inhibit high fructose feeding- or LPS-induced atherosclerosis through regulating oxidative stress, apoptosis and inflammation response in vivo and in vitro experiments. 50 and 100mg/kg quercetin were used in our study, showing significant inhibitory role in high fructose-induced atherosclerosis via reducing reactive oxygen species (ROS) levels, Caspase-3 activation, inflammatory cytokines releasing, the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells and collagen contents as well as modulating apoptosis- and inflammation-related proteins expression. We also explored the protective effects of quercetin on atherosclerosis by phosphatidylinositide 3-kinases (PI3K)/Protein kinase B (AKT)-associated Bcl-2/Caspase-3 and nuclear factor kappa B (NF-κB) signal pathways activation, promoting AKT and Bcl-2 expression and reducing Caspase-3 and NF-κB activation. Quercetin reduced the atherosclerotic plaque size in vivo in high fructose feeding-induced mice assessed by oil red O. Also, in vitro experiments, quercetin displayed inhibitory role in LPS-induced ROS production, inflammatory response and apoptosis, which were linked with PI3K/AKT-regulated Caspase-3 and NF-κB activation. In conclusion, our results showed that quercetin inhibited atherosclerotic plaque development in high fructose feeding mice via PI3K/AKT activation regulated by ROS.

iRhom2 is involved in lipopolysaccharide-induced cardiac injury in vivo and in vitro through regulating inflammation response.

Heart is a complex assembly of many cell types constituting of myocardium, endocardium and epicardium that intensively communicate to each other in order to maintain the proper cardiac function. Previous research has demonstrated that lipopolysaccharide (LPS) can induce myocardial dysfunction. iRhom2 is encoded by the gene Rhbdf2, regulating inflammation via tumor necrosis factor-α (TNF-α). In this study, we attempted to investigate the role of iRhom2 in LPS-induced cardiac injury and clarify the potential mechanism. We found that in vivo cardiac histopathological changes were induced after LPS challenge, accompanied with increase of TNF-α, interleukin-1ß (IL-1ß), interleukin-18 (IL-18) and interleukin-6 (IL-6) in serum and in heart tissue samples, which was dependent on TLR-4/NF-κB activation. Of note, we found that iRhom2 was a positive regulator for LPS-induced inflammation. LPS treatment markedly up-regulated iRhom2 and its down-streaming signal of IGS56. iRhom2 silence significantly suppress pro-inflammatory cytokines releases, and inactivated Toll-like receptor-4/Nuclear Factor kappa-B (TLR-4/NF-κB) signaling pathway in cells after LPS administration, suggesting its possible relationship with heart injury via TLR-4/NF-κB. It is concluded that iRhom2 may be a promising therapeutic target for LPS-induced cardiac injury by regulating inflammatory response.

Circulating miR-122-5p as a potential novel biomarker for diagnosis of acute myocardial infarction.

BACKGROUND: MicroRNAs (miRNAs) play key roles in cardiac development, and the expression of miRNAs is altered in the diseased heart. The aim of this study was to explore the value of circulating microRNA-122-5p (miR-122-5p) as a potential biomarker for acute myocardial infarction (AMI). METHODS: Plasma samples from 50 patients with AMI and 39 healthy adults (non-AMI controls) were collected. The abundance of circulating miR-122-5p was measured using quantitative real-time PCR (qRT-PCR). The cTnI concentrations of these samples were analyzed by ELISA. RESULTS: Our findings revealed that circulating miR-122-5p expression were increased in AMI patients at 4 h, 8 h, 12 h, and 24 h by contrast to those non-AMI controls and displayed similar trends to that of cTnI concentrations in AMI patients. Further study showed that there is a high correlation between circulating miR-122-5p and cTnI concentrations. At last, the receiver operating characteristic (ROC) curve was performed and showed that circulating miR-122-5p had considerable diagnostic accuracy for AMI with an area under curve (AUC) of 0.855. CONCLUSIONS: Our results implied that circulating miR-122-5p could be a potential biomarker for AMI.

[Association between metabolic syndrome and incidence of atrial fibrillation in essential hypertensive patients without left ventricular hypertrophy].

OBJECTIVE: To investigate the association between metabolic syndrome (MS) and the incidence of atrial fibrillation (AF) in essential hypertensive (EH) patients without left ventricular hypertrophy. METHODS: A total of 972 EH without left ventricular hypertrophy were divided into EH + non MS group (n = 606) and EH + MS group (n = 366). Incidence of AF were compared between two groups. RESULTS: (1) Incidence of AF in EH + MS group was significantly higher than that in EH + non MS group (12.84% vs. 6.93%, P < 0.01). (2) Left atrial diameter (LAD), left ventricular end-diastolic diameter (LVEDd), interventricular septum thickness (IVS), left ventricular posterior wall thickness (LVPW) and left ventricular mass (LVM) were all significantly higher in EH + MS group than those in EH + non MS group (all P < 0.01) while left ventricular mass index (LVMI) and ejection fraction (EF) were similar between two groups. (3) Logistic regression analysis showed age, hypertension duration, LAD, LVEDd and MS were significantly correlated with incidence of AF in EH patients (OR: 1.683, 1.308, 2.262, 3.848 and 1.853, P < 0.05) and obesity was the independent predictor for incidence of AF (OR: 1.706, P = 0.029). CONCLUSION: MS was associated with increased incidence of AF in EH patients without left ventricular hypertrophy in this cohort.