Region are exposed to factors and signals that indicate that tissue homeostasis and the integrity of the blood�Cbrain barrier has been disrupted. Which components present in the serum, or which signals released from neural and non-neural Folinic acid calcium salt pentahydrate elements are responsible for their increased proliferation and/or fate decision, remains to be determined. Nevertheless, these factors are likely to activate the Notch-1 pathway, as suggested by its up-regulation in reactive glial cells after injury. A similar up-regulation was described for bone morphogenetic factor in the post-injury niche, and this factor was shown to drive the differentiation of polydendrocytes into astrocytes, while simultaneously its antagonist Noggin reverses this process. A very important role in controlling the proliferation and differentiation of polydendrocytes is also played by the b-catenin signaling pathway, which is strongly activated after cortical injury. It seems that information about massive ischemic injury is delivered to polydendrocytes in a large part of the CNS; however, only the directly exposed subpopulation of polydendrocytes responds to this pathology not only by proliferation, but also by differentiation into another cell types. Diatoms belong to the most abundant photosynthetic microorganisms on Earth accounting for about 40% of the primary production in the oceans. The ecological success of both planktonic and benthic diatoms is partly owed to their ability to tolerate and quickly acclimate to a rapidly changing light climate. Growth in fluctuating light intensities requires a fast responding photosynthetic machinery to protect the chloroplast from potential damage by excess energy absorption at saturating light intensities. Plants and algae have evolved a number of photoprotective Orbifloxacin mechanisms including the non-photochemical quenching of fluorescence, NPQ. NPQ mediates thermal dissipation of excess light energy absorbed by the light-harvesting antenna complex of photosystem II. NPQ is mainly controlled by the inter-conversion of epoxidized to de-epoxidized forms of xanthophyll carotenoids during the so-called xanthophyll cycle. The xanthophyll de-epoxidation is mediated by an enzyme, the deepoxidase, which is located in the lumen of the thylakoids, while the back-conversion is ensured by a stromal epoxidase. The light-dependent build-up of the transthylakoidal proton gradient and the subsequent acidification of the lumen is necessary for the binding of the de-epoxidase to the thylakoid membrane in order to get access to its xanthophyll substrate. This process is regulated by the protonation of a glutamic acid-rich domain located in the highly charged C-terminal part of the enzyme and by the protonation of histidine residues located in the lipocalin region. In diatoms, there are two XCs, one of them is identical to the XC found in higher plants, performing the de-epoxidation of violaxanthin to zeaxanthin via the intermediate antheraxanthin by the violaxanthin de-epoxidase. The other and main XC of diatoms includes only a single step, the de-epoxidation of diadinoxanthin into diatoxanthin. The pigments of the Vx cycle are precursors of DD and DT, and of the main LHC xanthophyll, fucoxanthin. In diatoms, genes encoding for de-epoxidases assumed to be responsible for one or both XCs have been found. In Phaeodactylum tricornutum as well as in Thalassiosira pseudonana, there is a single gene encoding for a VDE protein, also named DDE with a strong similarity to the VDE of higher plants. Two additional proteins, named ‘VDE-like’ or VDL plus two ‘VDE-related’ or VDR in P. tricornutum are only distantly related.