No abstract

Photoinactivation of PSII is thought to be caused by the excessive light energy that is neither used for photosynthetic electron transport nor dissipated as heat. However, the relationship between the photoinactivation rate and excess energy has not been quantitatively evaluated. Chenopodium album L. plants grown under high-light and high-nitrogen (HL-HN) conditions show higher tolerance to photoinactivation and have higher photosynthetic capacity than the high-light and low-nitrogen (HL-LN)- and low-light and high-nitrogen (LL-HN)-grown plants. The rate of photoinactivation in the LL-HN plants was faster than that in the HL-LN, which was similar to that in the HL-HN plants, while the LL-HN and HL-LN plants had similar photosynthetic capacities [Kato et al. (2002b) Funct. Plant Biol. 29: 787]. We quantified partitioning of light energy between the electron transport and heat dissipation at the light intensities ranging from 300 to 1,800 micromol m(-2) s(-1). The maximum electron transport rate was highest in the HL-HN plants, heat dissipation was greatest in the HL-LN plants, and the excess energy, which was neither consumed for electron transport nor dissipated as heat, was greatest in the LL-HN plants. The first-order rate constant of the PSII photoinactivation was proportional to the magnitude of excess energy, with a single proportional constant for all the plants, irrespective of their growth conditions. Thus the excess energy primarily determines the rate of PSII photoinactivation. A large photosynthetic capacity in the HL-HN plants and a large heat dissipation capacity in the HL-LN plants both contribute to the protection of PSII against photoinactivation.

BackgroundThe global EINSTEIN DVT and PE studies compared rivaroxaban (15 mg twice daily for 3 weeks followed by 20 mg once daily) with enoxaparin/vitamin K antagonist therapy and demonstrated non-inferiority for efficacy and superiority for major bleeding. Owing to differences in targeted anticoagulant intensities in Japan, Japanese patients were not enrolled into the global studies. Instead, a separate study of deep vein thrombosis (DVT) and/or pulmonary embolism (PE) in Japanese patients was conducted, which compared the Japanese standard of care with a reduced dose of rivaroxaban.MethodsWe conducted an open-label, randomized trial that compared 3, 6, or 12 months of oral rivaroxaban alone (10 mg twice daily or 15 mg twice daily for 3 weeks followed by 15 mg once daily) with activated partial thromboplastin time-adjusted intravenous unfractionated heparin (UFH) followed by warfarin (target international normalized ratio 2.0; range 1.5–2.5) in patients with acute, objectively confirmed symptomatic DVT and/or PE. Patients were assessed for the occurrence of symptomatic recurrent venous thromboembolic events or asymptomatic deterioration and bleeding.ResultsEighty-one patients were assigned to rivaroxaban and 19 patients to UFH/warfarin. Three patients were excluded because of serious non-compliance issues. The composite of symptomatic venous thromboembolic events or asymptomatic deterioration occurred in 1 (1.4%) rivaroxaban patient and in 1 (5.3%) UFH/warfarin patient (absolute risk difference, 3.9% [95% confidence interval, -3.4–23.8]). No major bleeding occurred during study treatment. Clinically relevant non-major bleeding occurred in 6 (7.8%) patients in the rivaroxaban group and 1 (5.3%) patient in the UFH/warfarin group.ConclusionsThe findings of this study in Japanese patients with acute DVT and/or PE suggest a similar efficacy and safety profile with rivaroxaban and control treatment, consistent with that of the worldwide EINSTEIN DVT and PE program.Trial registrationClinicaltrials.gov: NCT01516840 and NCT01516814.Electronic supplementary materialThe online version of this article (doi:10.1186/s12959-015-0035-3) contains supplementary material, which is available to authorized users.

When given in addition to a RAS inhibitor, finerenone reduced albuminuria without adverse effects on serum potassium levels or renal function in Japanese patients with T2DM and DN.

Parameters for the evaluation of the effects of photoinhibition on photosynthetic carbon gain were studied in Chenopodium album leaves. The light‐response curve of photosynthetic rate was determined at 36 Pa CO2 partial pressure and fitted by a non‐rectangular hyperbola. Both the initial slope of the curve and the light‐saturated rate decreased in photoinhibited leaves, although the decrease in the latter was small. The convexity of the curve was also smaller in photoinhibited leaves. The capacities of ribulose‐1,5‐bisphosphate carboxylation (Vcmax) and electron transport (Jmax) were estimated from the CO2‐response curves. Vcmax and Jmax decreased similarly with increasing photoinhibition. Energy partitioning in photosystem II (PSII) was estimated using chlorophyll fluorescence parameters. The fraction of energy that was consumed by photochemistry decreased with increasing photoinhibition. However, an increase in inactive PSII, decreasing energy partitioning to active PSII, relaxed the excitation pressure in PSII, and led to a reduction in the fraction of excess energy that was neither consumed by photochemistry nor dissipated as heat.