Granular bacterial inoculant alters the rhizosphere microbiome and soil aggregate fractionation to affect phosphorus fractions and maize growth.

The constraint of phosphorus (P) fixation on crop production in alkaline calcareous soils can be alleviated by applying bioinoculants. However, the impact of bacterial inoculants on this process remains inadequately understood. Here, a field study was conducted to investigate the effect of a high-concentration, cost-effective, and slow-release granular bacterial inoculant (GBI) on maize (Zea mays L.) plant growth. Additionally, we explored the effects of GBI on rhizosphere soil aggregate physicochemical properties, rhizosphere soil P fraction, and microbial communities within aggregates. The outcomes showed a considerable improvement in plant growth and P uptake upon application of the GBI. The application of GBI significantly enhanced the AP, phoD gene abundance, alkaline phosphatase activity, inorganic P fractions, and organic P fractions in large macroaggregates. Furthermore, GBI impacted soil aggregate fractionation, leading to substantial alterations in the composition of fungal and bacterial communities. Notably, key microbial taxa involved in P-cycling, such as Saccharimonadales and Mortierella, exhibited enrichment in the rhizosphere soil of plants treated with GBI. Overall, our study provides valuable insight into the impact of GBI application on microbial distributions and P fractions within aggregates of alkaline calcareous soils, crucial for fostering healthy root development and optimal crop growth potential. Subsequent research endeavors should delve into exploring the effects of diverse GBIs and specific aggregate types on P fraction and community composition across various soil profiles.

Atractylon Treatment Attenuates Pulmonary Fibrosis via Regulation of the mmu_circ_0000981/miR-211-5p/TGFBR2 Axis in an Ovalbumin-Induced Asthma Mouse Model.

Asthma-induced pulmonary fibrosis (PF) is an important public health concern that has few treatment options given its poorly understood etiology; however, the epithelial to mesenchymal transition (EMT) of pulmonary epithelial cells has been implicated to play an important role in inducing PF. Although previous studies have found atractylon (Atr) to have anti-inflammatory effects, whether Atr has anti-PF abilities remains unknown. The purpose of the current study was to validate the protective efficiency of Atr in both an animal model of ovalbumin (OVA)-induced asthma and an EMT model induced by transforming growth factor-ß1 (TGF-ß1) using TC-1 cells. The results of this study revealed that Atr treatment suppressed OVA-induced PF via fibrosis-related protein expression. Atr treatment suppressed OVA-induced circRNA-0000981 and TGFBR2 expression but promoted miR-211-5p expression. In vivo studies revealed that Atr suppressed TGF-ß1-induced EMT and fibrosis-related protein expression via suppressing circRNA-0000981 and TGFBR2 expression. The results also suggested that the downregulation of circRNA-0000981 expression suppressed TGFBR2 by sponging miR-211-5p, which was validated by a luciferase reporter assay. Collectively, the findings of the present study suggest that Atr treatment attenuates PF by regulating the mmu_circ_0000981/miR-211-5p/TGFBR2 axis in an OVA-induced asthma mouse model.

TTF1­NP induces protective autophagy during apoptosis by inhibiting the Akt/mTOR pathway and activating JNK in human liver cancer cells.

TTF1­NP is a flavonoid nanoparticle based on 5,2',4'­trihydroxy­6,7,5'­trimethoxyflavone (TTF1), which is derived from the medicinal plant Sorbaria sorbifolia that grows in the Changbai Mountain. We previously demonstrated antitumor effects of TTF1­NP in human hepatoma including induction of apoptosis and inhibition of angiogenesis, migration and invasion. Herein, we examined the effects of TTF1­NP on autophagy and its relationship with apoptosis, and explored potential underlying mechanisms in human hepatoma cell lines. We conducted cell viability assays, Annexin V/propidium iodide double staining, Hoechst staining, monodansylcadaverine staining, transmission electron microscopy, green fluorescent protein­light chain 3 plasmid transfection and western blots. We found that TTF1­NP induced apoptosis and autophagy in HepG2 and SMMC­7721 cells. Pretreatment with the autophagy inhibitor 3­methyladenine promoted TTF1­NP­induced apoptosis. TTF1­NP decreased levels of phosphorylated (p)­Akt, p­mTOR and p­ERK1/2 and increased p­JNK levels in the two cell lines. Treating cells with insulin, SP600125 and U0126 indicated that the Akt/mTOR pathway and JNK were involved in TTF1­NP­induced autophagy. Together, these findings suggest that TTF1­NP induced protective apoptosis­related autophagy by modulating the Akt/mTOR and JNK pathways in HepG2 and SMMC­7721 cells. Therefore, autophagy may be a potential target for TTF1­NP in human hepatoma therapy.

TTF1, in the Form of Nanoparticles, Inhibits Angiogenesis, Cell Migration and Cell Invasion In Vitro and In Vivo in Human Hepatoma through STAT3 Regulation.

TTF1-NP (5,2',4'-trihydroxy-6,7,5'-trimethoxyflavone nanoparticles), derived from the traditional Changbai Mountain medicinal plant Sorbaria sorbifolia (SS), has been showed its anti-cancer effect in various liver cancer cell types and tissues. The present study was designed to evaluate the antitumor mechanism of the TTF1-NP against HepG2 hepatoma cells and HepG2 cells-induced hepatocarcinoma (HCC) in nude mouse model. Here we demonstrated that TTF1-NP inhibits tube formation of HUVECs and HepG2 cell migration and invasion, and inhibits tumor growth in nude mice implanted with HepG2 cells through the downregulation of STAT3 protein and activation, along with VEGF, KDR, bFGF, MMP2 and MMP9 levels. We further revealed that TTF1-NP decreased the DNA-binding capacity of STAT3. Together our results provide a mechanism by which TTF1-NP suppresses cancer cell migration, invasion and angiogenesis through the action of STAT3 and suggests TTF1-NP as a potential therapy for hepatocellular cancer treatment.

Distribution and temporal trend of polybrominated diphenyl ethers in one Shanghai municipal landfill, China.

The scarcity of information on polybrominated diphenyl ethers' (PBDEs) flow in landfill restricts the life cycle analysis of PBDEs. In this study, eight PBDE congeners (BDEs 28, 47, 99, 100, 153, 154, 183, and 209) in topsoil, vegetation leaves, leachate, and municipal aged refuse collected from Shanghai Laogang Municipal Landfill (SLML) were investigated. The present study revealed elevated PBDE concentrations in topsoil and proved PBDE leakage from SLML and vegetation uptake. BDE-209 was the predominant congener, and this could be due to massive usage of deca-BDE mixture in Shanghai. ΣPBDE concentrations in leachates treated by reed wetland and A(2)/O process fell in the low end of the worldwide range. ΣPBDE concentrations in aged refuse samples rose from under 50 ng/g dw in 1989 to the range of 5,150-5,718 ng/g dw in 2002. PBDE concentrations increase in aged refuse samples throughout the 1990s into the 2000s paralleled municipal solid waste output from 1991 to 2002 in Shanghai. Exponential increase in BDE-209 concentration in aged refuse suggested the increasing market demands for deca-BDE mixture after 1990 in China. Notably, the inventory of PBDEs in SLML was 28.7 MT, and the doubling time of BDE-209 in aged refuse was calculated to be 1.6 year. SLML can be considered as a source of PBDE and one main recipient of PBDE as well, receiving inputs predominantly from the PBDE-containing waste. Priority should be given to formulate regulation on PBDEs and sorting work before landfill disposal.