Since the 1970s, extensive croplands were converted to forest and pasture lands to control severe soil erosion on the Loess Plateau of China. We quantify the direct and indirect effects of vegetation restoration on runoff and sediment yield on hillslopes in the field to improve environmental governance.
Methods
An artificial rainfall experiment at a rainfall intensity of 120 mm h−1 and a slope gradient of 22° were used to distinguish the effects of vegetation restoration on runoff and sediment yield.
Results
Compared to the farmland slopes, vegetation restoration directly prolonged the time-to-runoff by 140%, reduced the runoff rate by 20%, and increased the soil infiltration capacity by 15%. Vegetation restoration indirectly delayed the time-to-runoff by 120%, reduced the runoff rate and sediment yield rate by 50% and 94%, respectively, and increased the soil infiltration capacity by 58% on the hillslopes with vegetation restoration.
Conclusions
The direct effects of vegetation restoration on runoff and sediment yield were lower than its indirect impacts. Vegetation cover, decreases in soil bulk density, and increases in belowground root biomasses and > 0.25 mm aggregate stability were the primary causes of runoff and sediment yield reduction on the slopes with vegetation restoration.
This study investigated the role of microRNA-95 (miR-95) in gastric cancer (GC) and to elucidate the underlying mechanism. Initially, bioinformatic prediction was used to predict the differentially expressed genes and related miRNAs in GC. miR-95 and DUSP5 expression was altered in GC cell line (MGC803) to evaluate their respective effects on the epithelial–mesenchymal transition (EMT) process, cellular processes (cell proliferation, migration, invasion, cell cycle, and apoptosis), cancer stem cell (CSC) phenotype, as well as tumor growth ability. It was further predicted in bioinformatic prediction and verified in GC tissue and cell line experiments that miR-95 was highly expressed in GC. miR-95 negatively regulated DUSP5, which resulted in the MAPK pathway activation. Inhibited miR-95 or overexpressed DUSP5 was observed to inhibit the levels of CSC markers (CD133, CD44, ALDH1, and Lgr5), highlighting the inhibitory role in the CSC phenotype. More important, evidence was obtained demonstrating that miR-95 knockdown or DUSP5 upregulation exerted an inhibitory effect on the EMT process, cellular processes, and tumor growth. Together these results, miR-95 knockdown inhibited GC development via DUSP5-dependent MAPK pathway. 相似文献
The aim of this work was to investigate the effects of age-related sarcopenia on the time and frequency domain properties of lower extremity muscles’ electromyographic and mechanomyographic activities. Healthy elderly (n=10, 64.5±4.5 yr) and young (n=10, 22.6±2.8 yr) were recruited as participants. Participants’ lean thigh volumes (LTV) and 1 RM (one repetition maximum) leg strength of quadriceps and maximum speed knee extension with different load levels (45%, 60% and 75% 1 RM) were recorded. The root mean square (RMS) and the mean frequency (MF) of the surface electromyography (EMGRMS, EMGMF) and mechanomyography (MMGRMS, MMGMF) signals were collected at vastus lateralis during concentric contraction with different intensity levels. Compared to the young, the elderly had significantly less LTV, absolute and relative maximal force, as well as absolute and relative maximal power (p<.05). EMGMF of the elderly and the young increased monotonically from 45% to 75% 1 RM testing conditions. While the MMGRMS of the young increased with testing intensities, the MMGRMS of the elderly increased only from 45% to 60% but leveled off from 60% to 75% 1 RM testing conditions. The results indicate the declines of muscle mass, force and power production capacity with aging. The observations could be explained by neuromuscular performance and change of MU activation patterns may result from age-related sarcopenia. Aging affected muscle power more than muscle strength, which could be due to fast fiber reduction. This is supported by our observations that the MMGRMS differences between the young and the elderly across all three intensity level where EMGRMS was only different at the greatest intensity. We suggest that MMG could be used as an important measurement in studying muscle contraction in age-related sarcopenia. 相似文献
The large subunit of herpes simplex virus (HSV) ribonucleotide reductase (RR), RR1, contains a unique amino-terminal domain which has serine/threonine protein kinase (PK) activity. To examine the role of the PK activity in virus replication, we studied an HSV type 2 (HSV-2) mutant with a deletion in the RR1 PK domain (ICP10ΔPK). ICP10ΔPK expressed a 95-kDa RR1 protein (p95) which was PK negative but retained the ability to complex with the small RR subunit, RR2. Its RR activity was similar to that of HSV-2. In dividing cells, onset of virus growth was delayed, with replication initiating at 10 to 15 h postinfection, depending on the multiplicity of infection. In addition to the delayed growth onset, virus replication was significantly impaired (1,000-fold lower titers) in nondividing cells, and plaque-forming ability was severely compromised. The RR1 protein expressed by a revertant virus [HSV-2(R)] was structurally and functionally similar to the wild-type protein, and the virus had wild-type growth and plaque-forming properties. The growth of the ICP10ΔPK virus and its plaque-forming potential were restored to wild-type levels in cells that constitutively express ICP10. Immediate-early (IE) genes for ICP4, ICP27, and ICP22 were not expressed in Vero cells infected with ICP10ΔPK early in infection or in the presence of cycloheximide, and the levels of ICP0 and p95 were significantly (three- to sevenfold) lower than those in HSV-2- or HSV-2(R)-infected cells. IE gene expression was similar to that of the wild-type virus in cells that constitutively express ICP10. The data indicate that ICP10 PK is required for early expression of the viral regulatory IE genes and, consequently, for timely initiation of the protein cascade and HSV-2 growth in cultured cells. 相似文献
Chronic pancreatitis (CP), characterized by pancreatic fibrosis, is a recurrent, progressive and irreversible disease. Activation of the pancreatic stellate cells (PSCs) is considered a core event in pancreatic fibrosis. In this study, we investigated the role of hydrogen peroxide‐inducible clone‐5 (Hic‐5) in CP. Analysis of the human pancreatic tissue samples revealed that Hic‐5 was overexpressed in patients with CP and was extremely low in healthy pancreas. Hic‐5 was significant up‐regulated in the activated primary PSCs independently from transforming growth factor beta stimulation. CP induced by cerulein injection was ameliorated in Hic‐5 knockout (KO) mice, as shown by staining of tissue level. Simultaneously, the activation ability of the primary PSCs from Hic‐5 KO mice was significantly attenuated. We also found that the Hic‐5 up‐regulation by cerulein activated the NF‐κB (p65)/IL‐6 signalling pathway and regulated the downstream extracellular matrix (ECM) genes such as α‐SMA and Col1a1. Therefore, we determined whether suppressing NF‐κB/p65 alleviated CP by treating mice with the NF‐κB/p65 inhibitor triptolide in the cerulein‐induced CP model and found that pancreatic fibrosis was alleviated by NF‐κB/p65 inhibition. These findings provide evidence for Hic‐5 as a therapeutic target that plays a crucial role in regulating PSCs activation and pancreatic fibrosis. 相似文献