It is critical for spring wheat (Triticum aestivum L.) production in the semi-arid Loess Plateau to understand the impact of nitrogen (N) fertilizer on changes in N metabolism, photosynthetic parameters, and their relationship with grain yield and quality. The photosynthetic capacity of flag leaves, dry matter accumulation, and N metabolite enzyme activities from anthesis to maturity were studied on a long-term fertilization trial under different N rates [0 kg ha?1(N1), 52.5 kg ha?1 (N2), 105 kg ha?1 (N3), 157.5 kg ha?1 (N4), and 210 kg ha?1 (N5)]. It was observed that N3 produced optimum total dry matter (5407 kg ha?1), 1000 grain weight (39.7 g), grain yield (2.64 t ha?1), and protein content (13.97%). Our results showed that N fertilization significantly increased photosynthetic parameters and N metabolite enzymes at all growth stages. Nitrogen harvest index, partial productivity factor, agronomic recovery efficiency, and nitrogen agronomic efficiency were decreased with increased N. Higher N rates (N3–N5) maintained higher photosynthetic capacity and dry matter accumulation and lower intercellular CO2 content. The N supply influenced NUE by improving photosynthetic properties. The N3 produced highest chlorophyll content, photosynthetic rate, stomatal conductance and transpiration rate, grain yield, grain protein, dry matter, grains weight, and N metabolite enzyme activities compared to the other rates (N1, N2, N4, and N5). Therefore, increasing N rates beyond the optimum quantity only promotes vegetative development and results in lower yields.
Alkenal double bond reductases (DBRs) catalyze the NADPH-dependent reduction of the α,β-unsaturated double bond of many secondary metabolites. Two alkenal double bond reductase genes PaDBR1 and PaDBR2 were isolated from the liverwort species Plagiochasma appendiculatum. Recombinant PaDBR2 protein had a higher catalytic activity than PaDBR1 with respect to the reduction of the double bond present in hydroxycinnamyl aldehydes. The residue at position 56 appeared to be responsible for this difference in enzyme activity. The functionality of a C56 to Y56 mutation in PaDBR1 was similar to that of PaDBR2. Further site-directed mutagenesis and structural modeling suggested that the phenol ring stacking between this residue and the substrate was an important determinant of catalytic efficiency. 相似文献
Plant height is an important agronomic trait. Dramatic increase in wheat yield during the "green revolution" is mainly due to the widespread utilization of the Reduced height (Rht)-1gene. We analyzed the natural allelic variations of three homoeologous loci Rht-A1, Rht-B1, and Rht-D1 in Chinese wheat (Triticum aestivum L.) micro-core collections and the Rht-B1/D1 genotypes in over 1,500 bred cultivars and germplasms using a modified EcoTILLING. We identified six new Rht-A1 allelic variations (Rht-Alb-g), eight new Rht-B1 allelic variations (Rht-Blh-o), and six new Rht-D1 allelic variations (Rht-Dle-j). These allelic variations contain single nucleotide polymorphisms (SNPs) or small insertions and deletions in the coding or uncoding regions, involving two frame-shift mutations and 15 missenses. Of which, Rht-Dle and Rht-Dlh resulted in the loss of interactions of GID1-DELLA-GID2, Rht-Blicould increase plant height. We found that the Rht-Blh contains the same SNPs and 197 bp fragment insertion as reported in Rht-Blc. Further detection of Rht-Blh in Tibet wheat germplasms and wheat relatives indicated that Rht-Blc may originate from Rht-Blh. These results suggest rich genetic diversity at the Rht-1 loci and provide new resources for wheat breeding. 相似文献
Studies have shown that chronic exposure to ambient fine particulate matter (less than 2.5 µm in aerodynamic diameter, PM2.5) pollution induces insulin resistance through alterations in inflammatory pathways. It is critical to study how the immune system responds to this stimulant, which has been linked to cardiovascular and autoimmune diseases, but few studies have been focused on such involvement of both neutrophils and monocytes in a timely manner. We hypothesized that the neutrophil was involved in the inflammatory response to air pollution.
Methods and Results
C57BL/6 mice were exposed to PM2.5 or filtered air (6 hours/day, 5 days/week) for 5, 14, and 21 days, respectively, in Columbus, OH. At the end of each of the exposure periods, we investigated the inflammatory response through flow cytometry, histology, intravital microscopy, and real-time PCR. PM2.5-exposed mice demonstrated a significant inflammatory response after 5 days of exposure. In the lung tissue and bronchoalveolar lavage fluid, monocytes/macrophages showed a transient response, while neutrophils showed a cumulative response. In addition, exposure to PM2.5 resulted in elevation of the monocyte chemoattractant protein 1 (MCP-1) cytokine, a monocyte/macrophage attractant in blood, at an early stage of exposure.
Conclusions
These findings suggest that PM2.5 exposure induces the inflammatory responses from both macrophages and neutrophils involvement. 相似文献
Several QSAR (quantitative structure-activity relationships) models for predicting the inhibitory activity of 117 Aurora-A kinase inhibitors were developed. The whole dataset was split into a training set and a test set based on two different methods, (1) by a random selection; and (2) on the basis of a Kohonen’s self-organizing map (SOM). Then the inhibitory activity of 117 Aurora-A kinase inhibitors was predicted using multilinear regression (MLR) analysis and support vector machine (SVM) methods, respectively. For the two MLR models and the two SVM models, for the test sets, the correlation coefficients of over 0.92 were achieved. 相似文献
Modulator compounds intended to overcome disease-causing mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) show significant promise in clinical testing for cystic fibrosis. However, the mechanism(s) of action underlying these compounds are not fully understood. Activation of CFTR ion transport requires PKA-regulated phosphorylation of the regulatory domain (R-D) and dimerization of the nucleotide binding domains. Using a newly developed assay, we evaluated nine compounds including both CFTR potentatiators and activators discovered via various high-throughput screening strategies to acutely augment CFTR activity. We found considerable differences in the effects on R-D phosphorylation. Some (including UC(CF)-152) stimulated robust phosphorylation, and others had little effect (e.g., VRT-532 and VX-770). We then compared CFTR activation by UC(CF)-152 and VRT-532 in Ussing chamber studies using two epithelial models, CFBE41o(-) and Fischer rat thyroid cells, expressing various CFTR forms. UC(CF)-152 activated wild-type-, G551D-, and rescued F508del-CFTR currents but did not potentiate cAMP-mediated CFTR activation. In contrast, VRT-532 moderately activated CFTR short-circuit current and strongly potentiated forskolin-mediated current. Combined with the result that UC(CF)-152, but not VRT-532 or VX-770, acts by increasing CFTR R-D phosphorylation, these findings indicate that potentiation of endogenous cAMP-mediated activation of mutant CFTR is not due to a pathway involving augmented R-D phosphorylation. This study presents an assay useful to distinguish preclinical compounds by a crucial mechanism underlying CFTR activation, delineates two types of compound able to acutely augment CFTR activity (e.g., activators and potentiators), and demonstrates that a number of different mechanisms can be successfully employed to activate mutant CFTR. 相似文献
Carvedilol is one of the most effective beta blockers for preventing ventricular tachyarrhythmias in heart failure, but the mechanisms underlying its favorable antiarrhythmic benefits remain unclear. Spontaneous Ca(2+) waves, also called store overload-induced Ca(2+) release (SOICR), evoke ventricular tachyarrhythmias in individuals with heart failure. Here we show that carvedilol is the only beta blocker tested that effectively suppresses SOICR by directly reducing the open duration of the cardiac ryanodine receptor (RyR2). This unique anti-SOICR activity of carvedilol, combined with its beta-blocking activity, probably contributes to its favorable antiarrhythmic effect. To enable optimal titration of carvedilol's actions as a beta blocker and as a suppressor of SOICR separately, we developed a new SOICR-inhibiting, minimally beta-blocking carvedilol analog, VK-II-86. VK-II-86 prevented stress-induced ventricular tachyarrhythmias in RyR2-mutant mice and did so more effectively when combined with either of the selective beta blockers metoprolol or bisoprolol. Combining SOICR inhibition with optimal beta blockade has the potential to provide antiarrhythmic therapy that can be tailored to individual patients. 相似文献
AimsHigh-fat diet (HFD) is associated with adipose inflammation, which contributes to key components of metabolic abnormalities. The expanded adipose tissue mass associated with obesity is the result of hyperplasia and hypertrophy of adipocytes. In this study, we investigated the effects of long-term HFD on adipocyte progenitor cell (APC) population and adipose-specific gene profiles in both white and brown adipose, and the role of perivascular adipose in the alteration of vascular function in response to HFD.Main methodsMale C57BL/6 mice were fed a standard normal diet (ND) or HFD for about 8 months. Glucose metabolism was assessed by an intraperitoneal glucose tolerance test. APC population and adipose-related gene profile were evaluated, and vascular function was measured in the presence or absence of perivascular adipose. Adiponectin and AMPK activity were also investigated.Key findingsHFD induced insulin resistance and glucose intolerance, and resulted in a decrease in APC population in brown, but not in white adipose tissue, when compared with animals fed a ND, with differential alterations of white and brown adipocyte-specific gene expression in brown and white adipose. Additionally, HFD led to altered vascular function in arteries in the presence of perivascular adipose tissue, which is associated with increased superoxide production. Adiponectin and AMPK activity were significantly decreased in response to long-term HFD.SignificanceThese findings suggest that long-term high-fat intake differentially alters adipocyte progenitor population and adipose-related gene expression in adipose tissue, and adiponectin-AMPK signaling might be involved. In addition, HFD induces changes in perivascular adipose-mediated vascular function. 相似文献