A review of ammonia-oxidizing bacteria and archaea in Chinese soils

Ammonia (NH3) oxidation, the first and rate-limiting step of nitrification, is a key step in the global Nitrogen (N) cycle. Major advances have been made in recent years in our knowledge and understanding of the microbial communities involved ammonia oxidation in a wide range of habitats, including Chinese agricultural soils. In this mini-review, we focus our attention on the distribution and community diversity of ammonia-oxidizing bacteria (AOB) and ammonia oxidizing archaea (AOA) in Chinese soils with variable soil properties and soil management practices. The niche differentiation of AOB and AOA in contrasting soils have been functionally demonstrated using DNA-SIP (stable isotope probing) methods, which have shown that AOA dominate nitrification processes in acidic soils, while AOB dominated in neutral, alkaline and N-rich soils. Finally, we discuss the composition and activity of ammonia oxidizer in paddy soils, as well as the mitigation of the greenhouse gas nitrous oxide (N2O) emissions and nitrate leaching via inhibition of nitrification by both AOB and AOA

mGluR5 antagonism inhibits cocaine reinforcement and relapse by elevation of extracellular glutamate in the nucleus accumbens via a CB1 receptor mechanism.

Metabotropic glutamate receptor 5 (mGluR5) antagonism inhibits cocaine self-administration and reinstatement of drug-seeking behavior. However, the cellular and molecular mechanisms underlying this action are poorly understood. Here we report a presynaptic glutamate/cannabinoid mechanism that may underlie this action. Systemic or intra-nucleus accumbens (NAc) administration of the mGluR5 antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) dose-dependently reduced cocaine (and sucrose) self-administration and cocaine-induced reinstatement of drug-seeking behavior. The reduction in cocaine-taking and cocaine-seeking was associated with a reduction in cocaine-enhanced extracellular glutamate, but not cocaine-enhanced extracellular dopamine (DA) in the NAc. MPEP alone, when administered systemically or locally into the NAc, elevated extracellular glutamate, but not DA. Similarly, the cannabinoid CB1 receptor antagonist, rimonabant, elevated NAc glutamate, not DA. mGluR5s were found mainly in striatal medium-spiny neurons, not in astrocytes, and MPEP-enhanced extracellular glutamate was blocked by a NAc CB1 receptor antagonist or N-type Ca++ channel blocker, suggesting that a retrograde endocannabinoid-signaling mechanism underlies MPEP-induced glutamate release. This interpretation was further supported by our findings that genetic deletion of CB1 receptors in CB1-knockout mice blocked both MPEP-enhanced extracellular glutamate and MPEP-induced reductions in cocaine self-administration. Together, these results indicate that the therapeutic anti-cocaine effects of mGluR5 antagonists are mediated by elevation of extracellular glutamate in the NAc via an endocannabinoid-CB1 receptor disinhibition mechanism

Oxygen uptake rate (OUR) control strategy for improving avermectin B1a production during fed-batch fermentation on industrial scale (150 m3)

Glucose metabolism plays a crucial role in the process of avermectin B1a biosynthesis. Controlling glucose feeding based on oxygen uptake rate (OUR) was established to improve the efficiency of avermectin B1a  production. The result showed that avermectin B1a production was greatly enhanced by OUR control strategy. In the glucose feeding phase, OUR was maintained at approximate 12 mmol/L/h, which was conducive to avermectin B1a biosynthesis. Using this OUR control strategy, an adequate supply of organic acid precursors produced avermectin B1a 5228 U/mL, which was 22.8% higher than that of the control (batch fermentation, 4256 U/mL) on industrial scale.Key words: Avermectin B1a, glucose feeding, oxygen uptake rate, industrial scale

ELISA for Aging Biomarkers Induced by Telomere Dysfunction in Human Plasma

Background. We identified cathelicidin related antimicrobial protein (CRAMP) secreted from telomere dysfunctional bone marrow cells of late generation telomerase knockout mice (G4mTerc−/−), increased in blood and various tissues. It can represented human aging and disease. The main aim of this study is to investigate the sensitive direct enzyme-linked immunosorbent assay (ELISA) method to analyze the human aging and disease in plasma and the detailed methods to quantify the direct ELISA of these aging biomarkers. Methods. Telomere lengths of 50 healthy persons are measured with real-time PCR in blood cells. Plasma samples from all subjects are analyzed using direct ELISA. Results. From 25 years old person to 78 years, the telomere length becomes shorter during aging. In blood plasma, the expression levels of CRAMP increases during human aging. There is the reverse correspondence between the telomere length and the plasma CRAMP level. We also find that the fresh plasma, the frozen plasma which thawed less than 3 times, and the plasma kept in the room temperature less than 3 hours are better for the ELISA analyze of CRAMP in the plasma. Conclusion. This CRAMP ELISA could become a powerful tool for investigating the relationship between human aging and telomere length shortening