Soil Available Nitrogen and Yield Effect under Different Combinations of Urease/Nitrate Inhibitor in Wheat/Maize Rotation System

In a wheat/maize rotation system, nitrogen (N) accounts for a large proportion of basal fertilizer, but soil N loss and the resulting environmental risk simultaneously exist worldwide. This study applied different urease/nitrification inhibitors together with basal fertilizers and investigated their effects on soil N level and grain yield. Six N stabilizing combinations consisted of two urease inhibitors (HQ and NBPT) and three nitrification inhibitors (DCD, DMPP, and Nitrapyrin). The treatments supplied with urease/nitrification inhibitors reduced, to some degree, the conversion rate of NH4+ into NO3−, and kept NH4+ content higher in surface soils for a longer time. Compared to CK, A1 treatment supplied with 1.5% HQ + 4% DCD well-maintained the levels of soil alkali-hydrolyzable N and NH4+. For example, alkali-hydrolyzable N and NH4+ contents at 0–20 cm soil layer under A1 were increased by 8.59–41.6% and 8.15–14.5% more than CK, respectively. Based on the entire growth period of wheat and maize rotation, urease/nitrification inhibitors improved soil available N in surface soils but did not prevent NH4+ and NO3− leaching, especially in the intensive rainfall season. The combinations of HQ and DCD or Nitrapyrin significantly enhanced crop yield. Specifically, crop yields under A1 and A3 (1.5% HQ + 0.25% Nitrapyrin) were 16.3% and 14.3% higher than CK, respectively. The N stabilizing combinations also promoted N intake and transport at every growth stage. The maximum N accumulation was increased by 27% under A1, when compared to CK. The treatments supplied with urease/nitrification inhibitors also achieved higher apparent N recovery efficiency, N agronomic efficiency, and N partial factor productivity. Consequently, the combinations of urease/nitrification inhibitors could improve N availability at 0–40 cm soil layer, which in turn improved N use efficiency of wheat and maize. The results suggested that the two urease/nitrification inhibitor combinations, 1.5% HQ + 4% DCD (A1) and 1.5% HQ + 0.25% Nitrapyrin (A3), were optimal N stabilizing agents and worthy of further study

Effect of ambient pressure on a femtosecond laser induced titanium plasma

Femtosecond laser induced Ti plasma has been characterized as a function of pressure by means of femtosecond laser induced breakdown spectroscopy (fs-LIBS). Experiments were performed with a Ti: sapphire laser system (100 fs, 800 nm), in an air pressure from 10 Pa to 104 Pa. The time-resolved spectrum has been acquired and the spectral intensities of different plasma species have been investigated with a changing ambient pressure. The Ti atomic lines decay while the ionic ones grow with an increasing pressure. The enhancement of nitrogen ionic line has also been observed. The time of flight spectroscopy is adopted to measure the expanding velocity of the plasma plume. The increasing pressure slows the plasma expansion along both axial and radial directions. The electron density and temperature are measured by means of Boltzmann plot method and Stark width method, respectively. It is concluded that higher pressure will increase the energy absorption and retard the plasma expansion, leading to larger electron density and temperature

Mechanisms of EGF Regulation of COX-2 Through the STAT5 Signaling Pathway in Human Lung Adenocarcinoma A549 Cells

Background and objective It has been proved that cyclooxygenase-2 (COX-2) is a key factor in lung cancer oncogenesis. COX-2 can be induced by a number of cytokines and growth factors and can be regulated by the JAK/STAT signaling pathway. Inhibiting the expression of COX-2 can prevent the development of lung cancer. The aim fo this study is to investigate whether the epidermal growth factor (EGF) can stimulate the signal transducers and activators of transcription 5 (STAT5) as well as to discover the effects of the STAT5 signaling pathway on the COX-2 in human lung adenocarcinoma A549 cells. Methods The phenomenon of STAT5 activation stimulated by the EGF was assayed through immunofluorescence and Western blot. The adenovirus containing the wild-type (WT)-STAT5 (AdWT-STAT5) plasmid, dominant-negative (DN)-STAT5 (Ad-CMV5Stat5aΔ740) plasmid, and STAT5 siRNA were transfected into A549 cells. The latter two groups were stimulated using EGF. Reverse transcriptase polymerase chain reaction was used to detect the mRNA expression of COX-2. Results STAT5 was not activated in A549 cells in vitro. EGF stimulation significantly increased the level of the p-STAT5 protein and induces the shuttling of p-STAT5 from the cytoplasm into the nucleus. STAT5 activation was crucial for the COX-2 expression induced by the EGF. STAT5 was required for COX-2 expression, but can mediated the effects of the COX-2 expression through pathways that were independent of transcriptional activation. Conclusion COX-2 expression is dependent on STAT5 phosphorylation. A second pathway does not require STAT5 phosphorylation