Long-term rice cultivation increases contributions of plant and microbial-derived carbon to soil organic carbon in saline-sodic soils.

Rice cultivation has been demonstrated to have the ability to improve saline-sodic soil. Whether this human activity can influence the accumulation of soil organic carbon (SOC) in saline-sodic soil remains unclear. In this study, the impact of rice cultivation across different planting durations (1, 5, 10, 27 years and abandoned land) on the carbon (C) levels, derived from plant residues and microbial necromass, were assessed. Compared to the control, plant residues and microbial necromass greatly contributed to the carbon accumulation. For the short-term of rice cultivation (1-10 years), the C content originated from both microbial and plant residues gradually accumulated. In the prolonged cultivation phase (27Y), plant residues and microbial necromasses contributed 40.82 % and 21.03 % of the total SOC, respectively. Additionally, rice cultivation significantly reduced the pH by 13.58-22.51 %, electrical conductivity (EC) by 60.06-90.30 %, and exchangeable sodium percentage (ESP) by 60.68-78.39 %. In contrast, total nitrogen (TN), total phosphorus (TP), SOC, particulate organic C, mineral-bound organic C, and microbial biomass all saw statistical increases. The activities of extracellular enzymes in paddy soils, such as peroxidase, phenol oxidase, and leucine aminopeptidase, were significantly reduced, and the decomposition of lignin, phenol, and amino sugars by soil microorganisms was consequently suppressed. The partial least squares path modeling results demonstrated that rice cultivation affected the accumulation of plant and microbial components via the corresponding chemical properties (pH, EC, and ESP), nutrient content (TN, TP, and SOC), enzyme activity (LAP, PER, and POX), microbial biomass, and plant biomass. These findings are crucial for understanding the organic carbon sequestration potential of sodic saline soils.

Nanoparticles for Stem Cell Tracking and the Potential Treatment of Cardiovascular Diseases.

Stem cell-based therapies have been shown potential in regenerative medicine. In these cells, mesenchymal stem cells (MSCs) have the ability of self-renewal and being differentiated into different types of cells, such as cardiovascular cells. Moreover, MSCs have low immunogenicity and immunomodulatory properties, and can protect the myocardium, which are ideal qualities for cardiovascular repair. Transplanting mesenchymal stem cells has demonstrated improved outcomes for treating cardiovascular diseases in preclinical trials. However, there still are some challenges, such as their low rate of migration to the ischemic myocardium, low tissue retention, and low survival rate after the transplantation. To solve these problems, an ideal method should be developed to precisely and quantitatively monitor the viability of the transplanted cells in vivo for providing the guidance of clinical translation. Cell imaging is an ideal method, but requires a suitable contrast agent to label and track the cells. This article reviews the uses of nanoparticles as contrast agents for tracking MSCs and the challenges of clinical use of MSCs in the potential treatment of cardiovascular diseases.

Toward green development? Impact of the carbon emissions trading system on local governments' land supply in energy-intensive industries in China.

Whether carbon emissions trading system promotes green development is important, especially from the land supply perspective. This paper investigates the effects of the carbon emissions trading pilot program on the land supply of the energy-intensive industries using the difference-in-difference approach, based on a big land-transaction dataset for the Chinese land market from 2007 to 2017. This paper finds that the carbon emissions trading program decreases the supply of energy-intensive industries' land by 25%, suggesting that it promotes the green development. Local governments' behavior affects the supply of energy-intensive industrial land. Industry structure dependence reinforce the effects of the carbon emissions trading program. The impacts of the carbon emissions trading program on the supply of energy-intensive industrial land would be less in cities with stronger regional competition, higher fiscal pressure or during political cycles. This study implies that the supply of energy-intensive industrial land can be used as an indicator for evaluating the effects of the carbon emissions trading system from the factor input perspective. The incentives of local government should be considered for understanding and assessing the effects of the carbon emissions trading system on land supply for future study.

Antioxidative nanofullerol inhibits macrophage activation and development of osteoarthritis in rats.

Background: There is emerging evidence which suggests that cellular ROS including nitric oxide (NO) are important mediators for inflammation and osteoarthritis (OA). Water-soluble polyhydroxylated fullerene C60 (fullerol) nanoparticle has been demonstrated to have an outstanding ability to scavenge ROS. Purpose: The objective of this study is to assess the effects of fullerol on inflammation and OA by in vitro and in vivo studies. Methods: For in vitro experiments, primary mouse peritoneal macrophages and a macrophage cell line RAW264.7 were stimulated to inflammatory phenotypes by lipopolysaccharide (LPS) in the presence of fullerol. For the animal study, OA model was created by intra-articular injection of monoiodoacetate into the knee joints of rats and fullerol was intravenously injected immediately after OA induction. Results: NO production and pro-inflammatory gene expression induced by LPS was significantly diminished by fullerol in both macrophage cell types. Meanwhile, fullerol could remarkably reduce phosphorylation of p38 mitogen-activated protein kinase, and protein level of transcription factors nuclear factor-kappaB and forkhead box transcription factor 1 within the nucleus. The animal study delineated that systematic administration of fullerol prevented OA, inhibiting inflammation of synovial membranes and the damage toward the cartilage chondrocytes in the OA joints. Conclusion: Antioxidative fullerol may have a potential therapeutic application for OA.

Triptolide inhibits the function of TNF-α in osteoblast differentiation by inhibiting the NF-κB signaling pathway.

Chronic inflammation often delays fracture healing or leads to bone nonunion. Effectively suppressing pathological inflammation is crucial for fracture healing or bone remodeling. Triptolide, which is a diterpenoid epoxide, is the major active component of the Thunder God Vine, Tripterygium wilfordii. The aim of the present study was to investigate the role of triptolide in osteoblast differentiation and explore the molecular mechanisms of triptolide in fracture healing. Alkaline phosphatase (ALP) activity was used to evaluate osteoblast differentiation. ALP activity was measured via histochemical staining and western blotting was used to determine the expression of factors associated with inflammation. C2C12 cells were initially treated with 200 ng/ml bone morphogenetic protein (BMP)-2 alone for 3 days, which caused a significant increase in ALP activity (P<0.01). However, treatment with tumor necrosis factor (TNF)-α significantly decreased the ALP activity (P<0.05). Notably, treatment with the chronic inflammatory cytokine TNF-α significantly decreased the effect of BMP-2 in C2C12 cells compared with BMP-2 treatment alone (P<0.01). C2C12 cells were treated with increasing concentrations of BMP-2 or TNF-α for 3 days. The results demonstrated that TNF-α treatment significantly inhibited BMP-2-induced osteoblast differentiation in a dose-dependent manner (P<0.01). The role of triptolide in BMP-2-induced osteoblast differentiation was also examined. Cells were treated with BMP-2, BMP-2 + TNF-α alone, or BMP2 + TNF-α with increasing concentrations of triptolide (4, 8 or 16 ng/ml). After 3 days, the results of ALP activity revealed that triptolide significantly reversed the TNF-α-associated inhibition of osteoblast differentiation (P<0.01). Western blotting analysis demonstrated that triptolide markedly inhibited the phosphorylation of nuclear factor-κB, therefore suppressing the effects of TNF-α. In summary, triptolide is able to reverse the TNF-α-associated suppression of osteoblast differentiation, suggesting that triptolide treatment may have a positive effect on bone remodeling and fracture repairing.

Targeting formyl peptide receptor 1 of activated macrophages to monitor inflammation of experimental osteoarthritis in rat.

Macrophages play a crucial role in the pathogenesis of osteoarthritis (OA). In this study, the feasibility of a formyl peptide receptor 1 (Fpr1)-targeting peptide probe cFLFLF-PEG-(64) Cu via positron emission tomography (PET) imaging was investigated for detection of macrophage activity during development of OA. Monoiodoacetate (MIA) was intraarticularly injected into the knee joint of Sprague-Dawley rats to induce OA. Five days later, cFLFLF-PEG-(64) Cu (∼7,400 kBq/rat) was injected into the tail vein and microPET/CT imaging was performed to assess the OA inflammation by detecting infiltration of macrophages by Fpr1 expression. In addition, a murine macrophage cell line RAW264.7 and two fluorescent probes cFLFLF-PEG-cyanine 7 (cFLFLF-PEG-Cy7) and cFLFLF-PEG-cyanine 5 (cFLFLF-PEG-Cy5) were used to define the binding specificity of the peptide to macrophages. It was found with the MIA model that the maximal standard uptake values (SUVmax ) for right (MIA treated) and left (control) knees were 17.96 ± 5.45 and 3.00 ± 1.40, respectively. Histological evaluation of cryomicrotome sections showed that Fpr1 expression, cFLFLF-PEG-Cy5 binding, and tartrate-resistant acid phosphatase activity were elevated in the injured synovial membranes. The in vitro experiments demonstrated that both fluorescent peptide probes could bind specifically to RAW264.7 cells, which was blocked by cFLFLF but not by the scramble peptide. The findings highlighted the use of cFLFLF-PEG-(64) Cu/PET as an effective method potentially applied for detection and treatment evaluation of OA. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 34:1529-1538, 2016.

[Effects of Ginseng and Sanchi Compositions on the Ras signal transduction pathway of myocardial ischemic rats].

OBJECTIVE: To study the effects of Ginseng and Sanchi Compositions (GSC) on the protein and mRNA expressions of Ras, extracellular signal-regulated Kinase1/2 (ERK1/2), and C-Raf-1 of ischemic myocardium of rats with acute myocardial infarction (AMI). METHODS: By adopting myocardial ischemia Wistar rat model with the ligation of the left anterior descending coronary artery, the normal control group, the sham-operation group, the model group, the Betaloc group, the high and low dose GSC group were set up. The protein expressions of Ras, C-Raf-1, ERK1/2,and phosphor-ERK1/2, p-ERK1/2 (p-ERK1/2) were detected by Western blot. The mRNA expressions of Ras, C-Raf-1, ERK1, and ERK2 were detected using Real-time PCR. RESULTS: The protein expressions of Ras, c-Raf-1, and p-ERK1/2 and their mRNA expressions in the model group increased more than those in the normal control group and the sham-operation group (P < 0.05). The protein expressions of Ras, c-Raf-1, and p-ERK1/2 and their mRNA expressions in the high and low dose GSC groups and the Betaloc group were significantly higher than those in the model group (P < 0.05). The protein expressions of Ras, c-Raf-1, and p-ERK1/2 and their mRNA expressions increased more obviously in the high dose GSC group than in the low dose GSC group (P < 0.05). The ERK1/2 protein expression was not significantly different among all groups (P > 0.05). CONCLUSIONS: GSC could up-regulate the protein expressions and mRNA expressions of Ras, C-Raf-1, and p-ERK1/2. It suggested that GSC might promote the angiogenesis through Ras signal transduction pathway dose-dependently.

[Action target of ginseng and panax notoginseng extracts on angiogenesis signaling pathway].

OBJECTIVE: To investigate the action targets of ginseng (GS) and Panax notoginseng (PN), Chinese herbs for benefiting qi and activating blood circulation, on angiogenesis signaling pathway (VEGFR-2-Ras-MAPK) in human umbilical vein endothelial cells (HUVEC). METHODS: To block the signal pathway by turns, at the first, added the IC50 of VEGFR-2 inhibitor, SU5416, and detected its downstream signaling protein Ras, MAPK expression using Western Blot. Secondly, added the IC50 of the Ras inhibitor, FPP, and detected its downstream signaling protein MAPK expression. RESULTS: Compared with the control group, adding SU5416 made the Ras, MAPK expression significantly decreased (P < 0.05, P < 0.01); and adding FPP made the expression of MAPK significantly decreased (P < 0.01). Compared with the group treated by SU5416 alone, the expression of downstream signaling protein Ras, MAPK were significantly higher in the group treated by SU5416 plus GS and PN (P < 0.05, P < 0.01); same state also found in comparison MAPK expression between groups treated with FPP alone and FPP plus GS and PN (P < 0.05). CONCLUSION: The angiogenesis mechanism of GS and PN on HUVEC may be realized by increasing the protein expression of three key signals, VEGFR-2, Ras and MAPK, respectively.

[Effects of Radix Ginseng and Radix Notoginseng formula on expressions of vascular endothelial growth factor receptor-2 and hypoxia-inducible factor-1alpha in ischemic myocardium of rats with acute myocardial infarction].

OBJECTIVE: To investigate the effects of Radix Ginseng and Radix Notoginseng formula on expressions of vascular endothelial growth factor receptor-2 (VEGFR-2) and hypoxia-inducible factor-1alpha (HIF-1alpha) in ischemic myocardium of rats with acute myocardial infarction. METHODS: A total of 100 Wistar rats were randomly divided into normal control group, sham-operated group, untreated group, metoprolol (Betaloc) group, and high- and low-dose Radix Ginseng and Radix Notoginseng formula groups. Acute myocardial infarction was induced in the untreated group, Betaloc group, and high- and low-dose Radix Ginseng and Radix Notoginseng formula groups by left anterior descending coronary artery ligation. After 12-day treatment, microvessel density (MVD) in ischemic myocardium was detected by immunohistochemical method, while expressions of VEGFR-2 and HIF-1alpha proteins were detected by Western blotting, and expressions of VEGFR-2 and HIF-1alpha mRNAs were detected by real-time fluorescent quantitative polymerase chain reaction. RESULTS: MVD in the untreated group was increased significantly, higher than those in the normal control group and the sham-operated group (P<0.05) and lower than those in the high- and low-dose Radix Ginseng and Radix Notoginseng formula groups and Betaloc group (P<0.01). VEGFR-2 and HIF-1alpha protein and mRNA expressions in the untreated group were higher than those in the normal control group and the sham-operated group (P<0.05). VEGFR-2 and HIF-1alpha protein and mRNA expressions in the high- and low-dose Radix Ginseng and Radix Notoginseng formula groups and Betaloc group were higher than those in the untreated group (P<0.05). There was a significant difference between the high- and low-dose Radix Ginseng and Radix Notoginseng formula groups (P<0.05). CONCLUSION: Radix Ginseng and Radix Notoginseng extract can up-regulate the protein and mRNA expressions of VEGFR-2 and HIF-1alpha and increase MVD in ischemic myocardium to improve myocardial ischemia so as to promote the development of collateral circulation.