Mechanisms of temperature acclimatisation in the psychrotolerant green alga Coccomyxa subellipsoidea C-169 (Trebouxiophyceae).

Despite the interest in different temperature acclimatisations of higher plants, few studies have considered the mechanisms that allow psychrotolerant microalgae to live in a cold environment. Although the analysis of the genomes of some algae revealed the presence of specific genes that encode enzymes that can be involved in the response to stress, this area has not been explored deeply. This work aims to clarify the acclimatisation mechanisms that enable the psychrotolerant green alga Coccomyxa subellipsoidea C-169 to grow in a broad temperature spectrum. The contents of various biochemical compounds in cells, the lipid composition of the biological membranes of entire cells, and the thylakoid fraction as well as the electron transport rate and PSII efficiency were investigated. The results demonstrate an acclimatisation mechanism that is specific for C. subellipsoidea and that allows the maintenance of appropriate membrane fluidity, for example, in thylakoid membranes. It is achieved almost exclusively by changes within the unsaturated fatty acid pool, like changes from C18:2 into C18:3 and C16:2 into C16:3 or vice versa. This ensures, for example, an effective transport rate through PSII and in consequence a maximum quantum yield of it in cells growing at different temperatures. Furthermore, reactions characteristic for both psychrotolerant and mesophilic microalgae, involving the accumulation of lipids and soluble sugars in cells at temperatures other than optimal, were observed. These findings add substantially to our understanding of the acclimatisation of psychrotolerant organisms to a wide range of temperatures and prove that this process could be accomplished in a species-specific manner.

Two isomorphous ZnII/CoII complexes with tri-tert-butoxysilanethiol and histamine, and (4-hydroxymethyl-1H-imidazole-kappaN)bis(tri-tert-butoxysilanethiolato-kappa2O,S)zinc(II).

The complexes [2-(1H-imidazol-4-yl-kappaN(3))ethylamine-kappaN]bis(tri-tert-butoxysilanethiolato-kappaS)cobalt(II), [Co(C(12)H(27)O(3)SSi)(2)(C(5)H(9)N(3))], and [2-(1H-imidazol-4-yl-kappaN(3))ethylamine-kappaN]bis(tri-tert-butoxysilanethiolato-kappaS)zinc(II), [Zn(C(12)H(27)O(3)SSi)(2)(C(5)H(9)N(3))], are isomorphous. The central Zn(II)/Co(II) ions are surrounded by two S atoms from the tri-tert-butoxysilanethiolate ligand and by two N atoms from the chelating histamine ligand in a distorted tetrahedral geometry, with two intramolecular N-H...O hydrogen-bonding interactions between the histamine NH(2) groups and tert-butoxy O atoms. Molecules of the complexes are joined into dimers via two intermolecular bifurcated N-H...(S,O) hydrogen bonds. The Zn(II) atom in [(1H-imidazol-4-yl-kappaN(3))methanol]bis(tri-tert-butoxysilanethiolato-kappa(2)O,S)zinc(II), [Zn(C(12)H(27)O(3)SSi)(2)(C(4)H(6)N(2)O)], is five-coordinated by two O and two S atoms from the O,S-chelating silanethiolate ligand and by one N atom from (1H-imidazol-4-yl)methanol; the hydroxy group forms an intramolecular hydrogen bond with sulfur. Molecules of this complex pack as zigzag chains linked by N-H...O hydrogen bonds. These structures provide reference details for cysteine- and histidine-ligated metal centers in proteins.

Functional magnetic resonance imaging within the rat spinal cord following peripheral nerve injury.

Functional magnetic resonance imaging (fMRI) was used to detect the effects of graded peripheral nerve injury at the spinal level. Graded peripheral nerve injury in rats was accomplished by transection of nerves entering the spinal cord at the L3 and L4 levels of the spinal cord segments. Electrical stimulation of the hindpaw was used to elicit activity within the spinal cord. The stimulation experimental paradigm consisted of 62 functional images, 5 slices each, with a total of 3 rest and 2 stimulation periods. A 9.4 T MRI system and a quadrature volume rf coil covering the lumbar spinal cord were used for the fMRI study. Sets of fast spin echo images were acquired repeatedly following sham preparatory surgery under control conditions and in rats following sham surgery (pre nerve cut), followed by L3 nerve and then L4 nerve section. In rats with sham surgery, there was a significant activation within the dorsal horn of slices corresponding to L3 and L4 spinal cord segments. Following section of the L3 nerve, there was a reduction in the number of active voxels in the L3 and L4 spinal cord segments. The activation was reduced further by sectioning of the L4 nerve. Thus, following an increasing loss of axonal connections to the spinal cord, there was a decreasing number of active voxels within the spinal cord. The results demonstrate that spinal fMRI in the rat has sufficient sensitivity to detect within the spinal cord the effects of a graded reduction in peripheral connectivity.

Application of magnetic resonance diffusion anisotropy imaging for the assessment neuroprotecting effects of MPEP, a selective mGluR5 antagonist, on the rat spinal cord injury in vivo.

Magnetic resonance diffusion anisotropy imaging (DAI) of the rat spinal cord after contusion using weight-drop method was used to study the neuroprotecting effect of 2-methyl-6-(phenylethynyl)-pyridine (MPEP), an mGluR5 receptor antagonist. Eighteen rats were used, divided into 3 groups of 6 animals: a reference group without any operation, a control group with injury and a test group with injury and MPEP. DAI was performed at 4.7 T at 1 h, 24 h, 48 h and 7 day after the injury. Locomotor function was evaluated using Basso, Beattie and Bresnahan (BBB) open field locomotor activity test each day starting one day after the injury. DAI results confirm positive effect of MPEP on the limitation of secondary excitotoxic injury in the spinal cord.

2-deoxyglucose induces beta-APP overexpression, tau hyperphosphorylation and expansion of the trans-part of the Golgi complex in rat cerebral cortex.

The effects of a single intraperitoneal injection of a non-metabolizable glucose analog 2-deoxyglucose (2-DG, 500 mg/kg) on the levels of beta-APP expression, and phosphorylated and unphosphorylated tau protein in the rat cerebral cortex were investigated. The effects of 2-DG on the ultrastructure of cortical neurons with particular emphasis on the morphology of the Golgi apparatus, and on brain bioenergetics assessed by in vivo 31P-MRS technique were also evaluated. Seven and a half hours after injection of 2-deoxyglucose a significant increase in brain cortex beta-APP expression, increased tau phosphorylation, and a marked relative expansion of the trans- part of the Golgi intracellular secretory pathway in cortical neurons has been found. The changes of beta-APP expression and tau phosphorylation appeared within 1 h after 2-DG application and continued for at least 24 h. However, brain 31P resonance spectra remained unchanged for up to 7.5 h after 2-DG. It is suggested that the increase of beta-APP expression represents a response of brain tissues to 2-DG-evoked biochemical stress, while tau hyperphosphorylation and the change in Golgi morphology may be secondary phenomena.