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Turku, Finland

The University of Turku , located in Turku in southwestern Finland, is the second largest university in the country as measured by student enrollment, after University of Helsinki. It was established in 1920 and also has faculties at Rauma, Pori and Salo. The university is a member of the Coimbra Group. Wikipedia.

Nikkanen L.,University of Turku
Philosophical transactions of the Royal Society of London. Series B, Biological sciences | Year: 2014

Plants have adopted a number of mechanisms to restore redox homeostasis in the chloroplast under fluctuating light conditions in nature. Chloroplast thioredoxin systems are crucial components of this redox network, mediating environmental signals to chloroplast proteins. In the reduced state, thioredoxins control the structure and function of proteins by reducing disulfide bridges in the redox active site of a protein. Subsequently, an oxidized thioredoxin is reduced by a thioredoxin reductase, the two enzymes together forming a thioredoxin system. Plant chloroplasts have versatile thioredoxin systems, including two reductases dependent on ferredoxin and NADPH as reducing power, respectively, several types of thioredoxins, and the system to deliver thiol redox signals to the thylakoid membrane and lumen. Light controls the activity of chloroplast thioredoxin systems in two ways. First, light reactions activate the thioredoxin systems via donation of electrons to oxidized ferredoxin and NADP(+), and second, light induces production of reactive oxygen species in chloroplasts which deactivate the components of the thiol redox network. The diversity and partial redundancy of chloroplast thioredoxin systems enable chloroplast metabolism to rapidly respond to ever-changing environmental conditions and to raise plant fitness in natural growth conditions. Source

Tyystjarvi E.,University of Turku
International Review of Cell and Molecular Biology | Year: 2013

Photoinhibition of Photosystem II (PSII) is the light-induced loss of PSII electron-transfer activity. Although photoinhibition has been studied for a long time, there is no consensus about its mechanism. On one hand, production of singlet oxygen (1O2) by PSII has promoted models in which this reactive oxygen species (ROS) is considered to act as the agent of photoinhibitory damage. These chemistry-based models have often not taken into account the photophysical features of photoinhibition-like light response and action spectrum. On the other hand, models that reproduce these basic photophysical features of the reaction have not considered the importance of data about ROS. In this chapter, it is shown that the evidence behind the chemistry-based models and the photophysically oriented models can be brought together to build a mechanism that confirms with all types of experimental data. A working hypothesis is proposed, starting with inhibition of the manganese complex by light. Inability of the manganese complex to reduce the primary donor promotes recombination between the oxidized primary donor and QA, the first stable quinone acceptor of PSII. 1O2 production due to this recombination may inhibit protein synthesis or spread the photoinhibitory damage to another PSII center. The production of 1O2 is transient because loss of activity of the oxygen-evolving complex induces an increase in the redox potential of QA, which lowers 1O2 production. © 2013 Elsevier Inc. Source

Yegutkin G.G.,University of Turku
Critical Reviews in Biochemistry and Molecular Biology | Year: 2014

Extracellular nucleotides and nucleosides mediate diverse signaling effects in virtually all organs and tissues. Most models of purinergic signaling depend on functional interactions between distinct processes, including (i) the release of endogenous ATP and other nucleotides, (ii) triggering of signaling events via a series of nucleotide-selective ligand-gated P2X and metabotropic P2Y receptors as well as adenosine receptors and (iii) ectoenzymatic interconversion of purinergic agonists. The duration and magnitude of purinergic signaling is governed by a network of ectoenzymes, including the enzymes of the nucleoside triphosphate diphosphohydrolase (NTPDase) family, the nucleotide pyrophosphatase/phosphodiesterase (NPP) family, ecto-5′-nucleotidase/CD73, tissue-nonspecific alkaline phosphatase (TNAP), prostatic acid phosphatase (PAP) and other alkaline and acid phosphatases, adenosine deaminase (ADA) and purine nucleoside phosphorylase (PNP). Along with "classical" inactivating ectoenzymes, recent data provide evidence for the co-existence of a counteracting ATP-regenerating pathway comprising the enzymes of the adenylate kinase (AK) and nucleoside diphosphate kinase (NDPK/NME/NM23) families and ATP synthase. This review describes recent advances in this field, with special emphasis on purine-converting ectoenzymes as a complex and integrated network regulating purinergic signaling in such (patho)physiological states as immunomodulation, inflammation, tumorigenesis, arterial calcification and other diseases. The second part of this review provides a comprehensive overview and basic principles of major approaches employed for studying purinergic activities, including spectrophotometric Pi-liberating assays, high-performance liquid chromatographic (HPLC) and thin-layer chromatographic (TLC) analyses of purine substrates and metabolites, capillary electrophoresis, bioluminescent, fluorometric and electrochemical enzyme-coupled assays, histochemical staining, and further emphasizes their advantages, drawbacks and suitability for assaying a particular catalytic reaction. © 2014 Informa Healthcare USA, Inc. Source

University of Turku | Date: 2015-09-15

A method for treating a compound semiconductor substrate, in which method in vacuum conditions a surface of an In-containing III-As, III-Sb or III-P substrate is cleaned from amorphous native oxides and after that the cleaned substrate is heated to a temperature of about 250-550 C. and oxidized by introducing oxygen gas onto the surface of the substrate. The invention relates also to a compound semiconductor substrate, and the use of the substrate in a structure of a transistor such as MOSFET.

An apparatus for determining information indicative of cardiac malfunctions and abnormalities includes a processing device (

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