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- Nilsson, Anders K., 1982, et al.
(författare)
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PSB33 protein sustains photosystem II in plant chloroplasts under UV-A light
- 2020
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Ingår i: Journal of Experimental Botany. - OXFORD ENGLAND : Oxford University Press (OUP). - 0022-0957 .- 1460-2431. ; 71:22, s. 7210-7223
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Tidskriftsartikel (refereegranskat)abstract
- Plants can quickly and dynamically respond to spectral and intensity variations of the incident light. These responses include activation of developmental processes, morphological changes, and photosynthetic acclimation that ensure optimal energy conversion and minimal photoinhibition. Plant adaptation and acclimation to environmental changes have been extensively studied, but many details surrounding these processes remain elusive. The photosystem II (PSII)-associated protein PSB33 plays a fundamental role in sustaining PSII as well as in the regulation of the light antenna in fluctuating light. We investigated how PSB33 knock-out Arabidopsis plants perform under different light qualities. psb33 plants displayed a reduction of 88% of total fresh weight compared to wild type plants when cultivated at the boundary of UV-A and blue light. The sensitivity towards UV-A light was associated with a lower abundance of PSII proteins, which reduces psb33 plants' capacity for photosynthesis. The UV-A phenotype was found to be linked to altered phytohormone status and changed thylakoid ultrastructure. Our results collectively show that PSB33 is involved in a UV-A light-mediated mechanism to maintain a functional PSII pool in the chloroplast.
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- Rysz, Susanne, et al.
(författare)
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The effect of levosimendan on survival and cardiac performance in an ischemic cardiac arrest model - A blinded randomized placebo -controlled study in swine
- 2020
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Ingår i: Resuscitation. - : Elsevier BV. - 0300-9572 .- 1873-1570. ; 150, s. 113-120
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Tidskriftsartikel (refereegranskat)abstract
- Background: Survival after out-of-hospital cardiac arrest remains poor. Levosimendan could be a new intervention in this setting. Therefore, we conducted a blinded, placebo controlled randomized study investigating the effects of levosimendan on survival and cardiac performance in an ischemic cardiac arrest model in swine. Methods: Twenty-four anesthetised swines underwent experimentally-induced acute myocardial infarction and ventricular fibrillation. At the start of CPR, a bolus dose of levosimendan (12 μg kg-1) or placebo was given followed by a 24-h infusion (0.2 μg kg-1 min-1) after return of spontaneously circulation. Animals were evaluated by risk of death, post-resuscitation hemodynamics and infarction size by magnetic resonance imaging (MRI) up to 32 h post arrest. Results: Spontaneous circulation was restored in all (12/12) animals in the levosimendan group compared to two thirds (8/12) in the placebo group (P = 0.09). Protocol survival was higher for the levosimendan group (P = 0.02) with an estimated 88% lower risk of death compared to placebo (hazard ratio [95% confidence interval] 0.12 [0.01-0.96], P = 0.046). Cardiac output (CO) recovered 40% faster during the first hour of the intensive care period for the levosimendan group (difference 0.13 [0.01-0.26] L min-1P = 0.04). The placebo group required higher inotropic support during the intensive care period which masked an even bigger recovery in CO in the levosimendan group (58%). The MRI showed no difference in myocardial scar size or in myocardial area at risk. Conclusions: Levosimendan given intra-arrest and during the first 24-h of post-resuscitation care improved survival and cardiac performance in this ischemic cardiac arrest model. Institutional Protocol Number; KERIC 5.2.18-14933.
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