Reactive oxygen species are an important element of redox regulation in cells and tissues. During physiological processes, molecules undergo chemical changes caused by reduction and oxidation reactions. Free radicals are involved in interactions with other molecules, leading to oxidative stress. Oxidative stress works two ways depending on the levels of oxidizing agents and products. Excessive action of oxidizing agents damages biomolecules, while a moderate physiological level of oxidative stress (oxidative eustress) is necessary to control life processes through redox signaling required for normal cellular operation. High levels of reactive oxygen species (ROS) mediate pathological changes. Oxidative stress helps to regulate cellular phenotypes in physiological and pathological conditions. Nrf2 (nuclear factor erythroid 2-related factor 2, NFE2L2) transcription factor functions as a target nuclear receptor against oxidative stress and is a key factor in redox regulation in hypertension and cardiovascular disease. Nrf2 mediates transcriptional regulation of a variety of target genes. The Keap1-Nrf2-ARE system regulates many detoxification and antioxidant enzymes in cells after the exposure to reactive oxygen species and electrophiles. Activation of Nrf2/ARE signaling is differentially regulated during acute and chronic stress. and Keap1 normally maintains Nrf2 in the cytosol and stimulates its degradation through ubiquitination. During acute oxidative stress, oxidized molecules modify the interaction of Nrf2 and Keap1, when Nrf2 is released from the cytoplasm into the nucleus where it binds to the antioxidant response element (ARE). This triggers the expression of antioxidant and detoxification genes. The consequence of long-term chronic oxidative stress is activation of glycogen synthase kinase 3β (GSK-3β) inhibiting Nrf2 activity and function. PPARγ (peroxisome proliferator-activated receptor gamma) is a nuclear receptor playing an important role in the management of cardiovascular diseases, hypertension and metabolic syndrome. PPARγ targeting of genes with peroxisome proliferator response element (PPRE) has led to the identification of several genes involved in lipid metabolism or oxidative stress. PPARγ stimulation is triggered by endogenous and exogenous ligands – agonists and it is involved in the activation of several cellular signaling pathways involved in oxidative stress response, such as the PI3K/Akt/NOS pathway. Nrf2 and PPARγ are linked together with their several activators and Nrf2/ARE and PPARγ/PPRE pathways can control several types of diseases.
Oxygen can afFect the photosynthetic processes in two antagonistic (protective and destructive) ways. The protection is represented by draining off of the electron transport systém, by utilisation of NADPH and ATP, and production of carbon dioxide in the process of photorespiration, oxygen reduction in the Mehler reaction, and also by regeneration of monodehydroascorbate, one of the fmal products of the Mehler-peroxidase reaction. The subsequent building up of the proton gradient in the Mehler and Mehler-peroxidase reactions also helps protéct the photosynthetic apparatus. The production of harmful oxygen radicals is accompanied by the Mehler reaction. This is in contrast to the fact that the Mehler reaction can also protéct the photosynthetic apparatus. Nevertheless, the scavenging mechanisms in plants are efficient enough for protection against the active oxygen species. In some cases the disproportion between the production and scavenging of active oxygen can result in the destruction of thylakoid membrane. Singlet oxygen, another toxic form of oxygen, can also significantly increase the inhibition of photosynthesis in the presence of oxygen. None of these processes works alone or independently, they are in a dynamic equilibrium and each of them contributes to the regulation of photosynthesis.
Flagellin (flg22) induces rapid and long-lasting defence responses. It may also affect the photosynthetic activity depending on several internal and external factors, such as the phytohormone ethylene or the day/night time. Based on the results, flg22 treatment, neither in the light phase nor in the evening, caused any significant change in chlorophyll fluorescence induction parameters in the leaves of wild-type and ethylene-receptor mutant Never ripe tomato plants measured the next morning. However, flg22 in the light phase decreased the effective quantum yield and the photochemical quenching both locally and systemically in guard cells. In parallel, the production of reactive oxygen species and nitric oxide increased, which contributed to the stomatal closure and a decrease in CO2 assimilation the next day. A decrease in sugar content and elevated hexokinase activity measured after flg22 exposure can also contribute to local defence responses in intact tomato plants.
Electroantennogram responses of the polyphagous leafminer Liriomyza sativae and its generalist parasitoid Diglyphus isaea to host and non-host plant odours of L. sativae were investigated. The odours of healthy leaves can elicit distinct EAG responses in L. sativae. The EAG responses to the odours of the host plants, bean and tomato, were stronger than to non-host plants, Chinese rose and morning glory. Neither healthy host nor non-host plants of the leafminer elicited distinctive EAG responses in the parasitoid, D. isaea. Odours of physically damaged leaves, no matter whether of host or non-host plants, increased strongly the EAG responses of the leafminer and its parasitoid. We compared the EAG responses of D. isaea to bean leaves of different status. The odour of mined leaves elicited distinct EAG responses, which were weaker than those of physically damaged ones. No differences were detected in the EAG response to leaves with empty mines, healthy leaves or an air control. The role of plant odours in host location of the leafminer and its parasitoid is discussed.
Recent host records for Gephyraulus raphanistri (Kieffer), a flower-gall midge, show restriction to Raphanus raphanistrum throughout Europe. Gephyraulus raphanistri has never been reported infesting commercially grown Brassica crops. Historical records showing a broad host range appear to have resulted from confusion with new or as yet undescribed Gephyraulus spp. and Contarinia nasturtii (Kieffer), a known gall-former of Brassica and other related genera. This study tested host specificity of G. raphanistri in the field in Europe by manipulating host plant phenology of actual and potential hosts in the genera Raphanus and Brassica as part of a risk assessment of the insect as a potential biological control agent of R. raphanistrum, one of the most important weeds of crops in Australia. Raphanus raphanistrum raphanistrum (wild radish), R. raphanistrum landra (coastal wild radish), Raphanus sativus (radish) and Brassica napus (oilseed rape cultivar) were phenologically synchronised for initial flowering and planted out in a flowering time and species block design near a natural population of R. r. landra hosting a natural population of G. raphanistri. Three generation peaks in gall formation were observed in the experiment, with galls developing on all test plants with an apparent preference for R. r. landra. The high field specificity of this gall midge is driven by the synchrony of oviposition and flower availability, not host physiological incompatibility or behavioural unacceptability. Commercially grown Brassica spp. are not suitable hosts for G. raphanistri because in the field they differ in flowering phenology from Raphanus raphanistrum. The overlap in the flowering phenology of the crop and weed in Australia makes this insect unsuitable as a biological control agent.
The peroxisome proliferator-activated receptors (PPAR) belong to the nuclear superfamily of ligand-activated transcription factors. PPARγ acts as a nutrient sensor that regulates several homeostatic functions. Its disruption can lead to vascular pathologies, disorders of fatty acid/lipid metabolism and insulin resistance. PPARγ can modulate several signaling pathways connected with blood pressure regulation. Firstly, it affects the insulin signaling pathway and endothelial dysfunction by modulation of expression and/or phosphorylation of signaling molecules through the PI3K/Akt/eNOS or MAPK/ET-1 pathways. Secondly, it can modulate gene expression of the renin- angiotensin system – cascade proteins, which potentially slow down the progression of atherosclerosis and hypertension.
Thirdly, it can modulate oxidative stress response either directly through PPAR or indirectly through Nrf2 activation. In this context, activation and functioning of PPARγ is very important in the regulation of several disorders such as diabetes mellitus, hypertens
ion and/or metabolic syndrome.
In this paper, I argue that the notion of ''best explanation'', as it appears in the Inference to the Best Explanation (IBE), can be defined in terms of explanatory power (EP) (i.e. the best explanation among a set of possible explanations is the one having the highest EP), if we employ a probabilistic measure of EP, which takes into account both the likelihoods and the prior probabilities of the compared explanatory hypotheses. Although the association between the EP of a hypothesis and its likelihood is largely uncontroversial, most of those working on EP do not see an association between EP and the prior probability of an explanatory hypothesis. I provide three examples (two toy examples and one from real scientific practice), in order to show that the role of priors in decisions about the best explanatory hypothesis deserves a serious consideration. I also show that such an explication of ''best explanation'' allows us to compare IBE and Bayesian confirmation theory (BCT) in terms of the probabilities they assign to two competing hypotheses, and thus to elicit the conditions under which both IBE and BCT lead to the same conclusion and are in this sense compatible., V tomto příspěvku tvrdím, že pojem ,,nejlepší vysvětlení'', jak je uveden v Úmluvě k nejlepšímu vysvětlení (IBE), lze definovat z hlediska vysvětlující síly (EP) (tj. Nejlepší vysvětlení mezi množstvím možných vysvětlení je ta, která má nejvyšší EP), pokud použijeme pravděpodobnostní měřítko EP, které bere v úvahu jak pravděpodobnosti, tak i předchozí pravděpodobnosti porovnávaných vysvětlujících hypotéz. Ačkoli asociace mezi EP hypotézy a její pravděpodobností je do značné míry nekontroverzní, většina z těch, kteří pracují na EP, nevidí asociaci mezi EP a předchozí pravděpodobností vysvětlující hypotézy. Uvádím tři příklady (dvě příklady hraček a jednu ze skutečné vědecké praxe), aby bylo zřejmé, že role předchůdců v rozhodování o nejlepší vysvětlující hypotéze si zaslouží seriózní zvážení. Rovněž dokazuji, že takové vysvětlení ,,nejlepšího vysvětlení'' nám umožňuje porovnat IBE a Bayesovskou potvrzovací teorii (BCT) z hlediska pravděpodobností, které přiřazují dvěma konkurenčním hypotézám, a tak vyvolat podmínky, za kterých IBE i BCT vedou k stejný závěr a jsou v tomto smyslu slučitelné., and Anton Donchev
Protease-activated receptors (PARs) belong to the G-proteincoupled receptor family, that are expressed in many body tissues especially in different epithelial cells, mast cells and also in neurons and astrocytes. PARs play different physiological roles according to the location of their expression. Increased evidence supports the importance of PARs activation during nociceptive signaling and in the development of chronic pain states. This short review focuses on the role of PAR2 receptors in nociceptive transmission with the emphasis on the modulation at the spinal cord level. PAR2 are cleaved and subsequently activated by endogenous proteases such as tryptase and trypsin. In vivo, peripheral and intrathecal administration of PAR2 agonists induces thermal and mechanical hypersensitivity that is thought to be mediated by PAR2-induced release of pronociceptive neuropeptides and modulation of different receptors. PAR2 activation leads also to sensitization of transient receptor potential channels (TRP) that are crucial for nociceptive signaling and modulation. PAR2 receptors may play an important modulatory role in the development and maintenance of different pathological pain states and could represent a potential target for new analgesic treatments., P. Mrozkova, J. Palecek, D. Spicarova., and Obsahuje bibliografii
Podle knihy Petera Harrisona The Bible, Protestantism and the Rise of Natural Science z roku 1998 vznikla moderní věda jako výsledek důrazu protestantů na doslovný smysl Písma, jejich odmítnutí dřívějšího symbolického či alegorického výkladu a jejich snahy o fi xaci významu biblického textu, v němž každá pasáž měla mít jediný a jedinečný význam. Tento článek se pokouší o shrnutí nejvýznamnějších kritik Harrisonovy hypotézy (od Kennetha Howella, Jitse van der Meera a Richarda Oosterhoff a) a uznává jejich oprávněnost. Nicméně ani alternativní vysvětlení vzestupu moderní vědy jakožto výsledku neshod ve výkladu Písma a následného objevu nejednoznačné povahy běžného verbálního jazyka není zcela uspokojivé., According to Peter Harrison’s book The Bible, Protestantism and the Rise of Natural Science (1998) modern science came into existence as a result of the emphasis of Protestants on the literal sense of the Scripture, their refusal of the earlier symbolic or allegorical interpretation, and their efforts at fixing the meaning of the biblical text in which each passage was to be ascribed a single and unique meaning. This article tries to summarize the most significant critiques of Harrison’s hypothesis (by Kenneth Howell, Jiste van der Meer and Richard Oosterhoff) and to acknowledge their legitimacy. However, the alternative explanation of the emergence of modern science as a result of disputes over the biblical interpretation and the subsequent discovery of the ambiguous character of the ordinary verbal language is not fully satisfactory either., and Petr Pavlas.