Cuttings of P. przewalski were exposed to two different watering regimes which were watered to 100 and 25 % of field capacity (WW and WS, respectively). Drought stress not only significantly decreased net photosynthetic rate (P N ), transpiration rate (E), stomatal conductance (g s ), efficiency of photosystem 2 (PS2) (F v /F m and yield), and increased intrinsic water use efficiency (WUE i ) under controlled optimal conditions, but also altered the diurnal changes of gas exchange, chlorophyll fluorescence, and WUE i . On the other hand, WS also affected the P N -photosynthetically active radiation (PAR) response curve. Under drought stress, P N peak appeared earlier (at about 10:30 of local time) than under WW condition (at about 12:30). At midday, there was a depression in P N for WS plants, but not for WW plants, and it could be caused by the whole microclimate, especially high temperature, low relative humidity, and high PAR. There were stomatal and non-stomatal limitations to photosynthesis. Stomatal limitation dominated in the morning, and low P N at midday was caused by both stomatal and non-stomatal limitations, whereas non-stomatal limitation dominated in the afternoon. In addition, drought stress also increased compensation irradiance and dark respiration rate, and decreased saturation irradiance and maximum net photosynthetic rate. Thus drought stress decreased plant assimilation and increased dissimilation through affected gas exchange, the diurnal pattern of gas exchange, and photosynthesis-PAR response curve, thereby reducing plant growth and productivity.

A note on versions:The version presented here may differ from the published version or from the version of record. If you wish to cite this item you are advised to consult the publisher's version. Please see the repository url above for details on accessing the published version and note that access may require a subscription.For more information, please contact eprints@nottingham.ac.ukManuscript ID TPEL-Reg-2014-04-0475.R2 1  Abstract-Power electronics are efficient for conversion and conditioning of the electrical energy through a wide range of applications. Proper life consumption estimation methods applied for power electronics that can operate in real-time under inservice mission profile conditions will not only provide an effective assessment of the products life expectancy but also they can deliver reliability design information. This is important to aid in manufacturing and thus help in reducing costs and maximizing through-life availability. In this paper, a mission profile based approach for real-time life consumption estimation which can be used for reliability design of power electronics is presented. The paper presents the use of electro-thermal models coupled with physics-of-failure analysis by means of real-time counting algorithm to provide accurate life consumption estimations for power modules operating under in-service conditions. These models, when driven by the actual mission profiles, can be utilized to provide advanced warning of failures and thus deliver information that can be useful to meet particular application requirements for reliability at the design stage. To implement this approach, an example of two case studies using mission profiles of a metro-system and wind-turbines applications are presented.

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Tenuazonic acid (TeA), a nonhost-specific phytotoxin produced by Alternaria alternata, was determined to be a novel natural photosynthesis inhibitor owning several action sites in chloroplasts. To further elucidate the mode of its action, studies were conducted to assess the production and involvement of reactive oxygen species (ROS) in the toxic activity of TeA. A series of experiments indicated that TeA treatment can induce chloroplast-derived ROS generation including not only (1)O(2) but also superoxide radical, H(2)O(2) and hydroxyl radicals in Eupatorium adenophorum mesophyll cells, resulting from electron leakage and charge recombination in PSII as well as thylakoid overenergization due to inhibition of the PSII electron transport beyond Q(A) and the reduction of end acceptors on the PSI acceptor side and chloroplast ATPase activity. The initial production of TeA-induced ROS was restricted to chloroplasts and accompanied with a certain degree of chloroplast damage. Subsequently, abundant ROS were quickly dispersed throughout whole cell and cellular compartments, causing a series of irreversible cellular harm such as chlorophyll breakdown, lipid peroxidation, plasma membrane rupture, chromatin condensation, DNA cleavage, and organelle disintegration, and finally resulting in rapid cell destruction and leaf necrosis. These results show that TeA causing cell necrosis of host-plants is a result of direct oxidative damage from chloroplast-mediated ROS eruption.