Nitrous oxide emissions from tea plantations: A review.

Tea plantations are an important N2O source. Fertilizer-induced N2O emission factors of tea plantations are much higher than other upland agricultural ecosystems. According to the basic information on characteristics and knowledge of N2O emissions from tea plantations around the world, we comprehensively reviewed N2O emission characteristics, production process, influencing factors, and reduction measures from tea plantations. The global means of ambient N2O emission and N2O emission stimulated by nitrogen fertilizer application from tea plantations were (2.68±2.92) kg N·hm-2 and (11.29±9.45) kg N·hm-2, respectively. The fertilizer-induced N2O emission factor in tea plantations (2.2%±2.1%) was much higher than the IPCC-estimated N2O emission factor for agricultural land (1%). N2O emission from tea plantation soil (a typical acid soil) were mainly produced during nitrification and denitrification, with denitrification being dominant. N2O emission from tea plantations were significantly related to the amount of fertilizer application. Other factors, such as fertilizer type, could also affect soil N2O emissions in tea plantations. The main reduction methods of N2O emission from tea plantations included optimizing the amount and type of fertilizer, amending biochar, and rationally using nitrification inhibitors. In future, we should strengthen in-situ observations of soil N2O emission from tea plantations at both temporal and spatial scales, combine lab incubation and field studies to elucidate the mechanisms underling tea plantation soil N2O emissions, and use a data-model fusion approach to reduce uncertainties in the estimation of global N2O emission. These would provide theoretical support and practical guidance for reasonable N2O emission reduction in tea plantations.

Application of substrate utilization patterns and terminal restriction fragment length polymorphism analysis to characterize the oral bacterial community of healthy subjects and patients with periodontitis.

Understanding the association between the bacterial community and oral health status is essential for the diagnosis and therapy of periodontal diseases. The aim of the present study was to apply three methods [conventional culture, substrate utilization using the MicroResp™ system and terminal restriction fragment length polymorphism (T-RFLP)] to investigate the oral bacterial community in saliva from 20 healthy subjects and 20 patients with periodontitis. The three methods all revealed that there was a systematic change in the microbial ecological characteristics associated with oral health status. Compared with the control group, the oral bacterial flora in the patients with chronic periodontitis had a greater culturable population and altered preferred carbon source and TRFLP patterns. TRFLP analysis was found to give more information and exhibit a higher sensitivity than the substrate utilization and conventional culture methods. In conclusion, TRFLP analysis is a potentially rapid method to assess the composition of the oral microbial community and for the diagnosis of chronic periodontitis.

[Rapid screening of katG gene mutation in isoniazid-resistant Mycobacterium tuberculosis]

OBJECTIVE: To evaluate the relationship between katG gene mutation and isoniazid (INH) resistance and to develop a rapid screening method of point mutation in the katG gene associated with MTB resistance. METHODS: Twenty-four clinical isolates of MTB with 8 INH resigtance isolates and 16 INH-sensitive isolates were analyzed by PCR-RFLP, with the H(37)Rv reference strain as the control. RESULTS: G-->C point mutations were detected in 7 of 8 isoniazid-resistant strains and no gene mutation was shown in 16 isoniazid-sensitive isolates. The sensitivity and specificity were 87.5 % and 100 % respectively. No katG gene sequence deletion was observed in any specimen. CONCLUSION: Our results suggest katG gene mutation is one of the most important mechanisms of INH-resistant TB. PCR-RFLP may be useful in detection of katG gene mutation.