Morphological and Functional Modifications of Optical Thin Films for Space Applications Irradiated with Low-Energy Helium Ions.

Future space missions will operate in increasingly hostile environments, such as those in low-perihelion solar orbits and Jovian magnetosphere. This exploration involves the selection of optical materials and components resistant to the environmental agents. The conditions in space are reproduced on ground through the use of ion accelerators. The effects of He particles coming from the solar wind impinging on a gold thin film have been systematically investigated, considering absorbed doses compatible with the duration of the European Space Agency Solar Orbiter mission. Structural and morphological changes have been proved to be dependent not only on the dose but also on the irradiation flux. A predictive model of the variation of thin film reflectance has been developed for the case of lower flux irradiation. The results are discussed regarding reliability and limitations of laboratory testing. The outcomes are important to address the procedures for the space qualification tests of optical coatings.

The electronic properties of three popular high spin complexes [TM(acac)3, TM = Cr, Mn, and Fe] revisited: an experimental and theoretical study.

The occupied and unoccupied electronic structures of three high spin TM(acac)3 (TM = Cr, Mn, and Fe) complexes (I, II, and III, respectively) were studied by revisiting their literature vapour-phase He(i) and, when available, He(ii) photoemission (PE) spectra and by means of original near-edge X-ray absorption fine structure (NEXAFS) spectroscopic data recorded at the O K-edge (OK-edge) and TM L2,3-edges (TML2,3-edges). The assignments of the vapour-phase He(i)/He(ii) PE spectra were guided by the results of spin-unrestricted non-relativistic Slater transition state calculations, while the OK-edge and TML2,3-edge spectroscopic pieces of evidence were analysed by exploiting the results of spin-unrestricted scalar-relativistic time-dependent density functional theory (DFT) and DFT/ROCIS calculations, respectively. Although the actual symmetry (D3, in the absence of any Jahn-Teller distortion) of the title molecules allowed an extensive mixing between TM t2g-like and eg-like atomic orbitals, the use of the Nalewajski-Mrozek TM-O bond multiplicity index combined with a thorough analysis of the ground state (GS) outcomes allowed the assessment of the TM-O bond weakening associated with the progressive TM 3d-based eg-like orbital filling. The experimental information provided by OK-edge spectra was rather poor; nevertheless, the combined use of symmetry, orbitals and spectra allowed us (i) to rationalise minor differences characterizing spectral features along the series, (ii) to quantify the contribution provided by the ligand-to-metal-charge-transfer (LMCT) excitations to the different spectral features, and (iii) to recognize the t2g-/eg-like nature of the TM 3d-based orbitals involved in LMCT transitions. As far as the TML2,3-edge spectra and the DFT/ROCIS results were concerned, the lowest lying I,IIL3 spectral features included states having either the GS spin multiplicity (S(I) = 3/2, S(II) = 2) or, at higher excitation energies (EEs), states with ΔS = ±1. In contrast to that, only states with ΔS = 0, -1 significantly contributed to the IIIL3 spectral pattern. Along the whole series, the L3 higher EE side was systematically characterized by states involving TM2p → π4 MLCT excitations; as such, coupled-single excitations with ΔS = 0 were involved in I and II, while single MLCT TM2p → π4 transitions with ΔS = -1 were involved in III.

Role of cerebral inflammation after traumatic brain injury: a revisited concept.

Neuroinflammation occuring after traumatic brain injury (TBI) is a complex phenomenon comprising distinct cellular and molecular events involving the injured as well as the healthy cerebral tissue. Although immunoactivation only represents a one of the many cascades initiated in the pathophysiology of TBI, the exact function of each mediator, activated cell types or pathophysiological mechanism, needs to be further elucidated. It is widely accepted that inflammatory events display dual and opposing roles promoting, on the one hand, the repair of the injured tissue and, on the other hand, causing additional brain damage mediated by the numerous neurotoxic substances released. Most of the data supporting these hypotheses derive from experimental work based on both animal models and cultured neuronal cells. More recently, evidence has been provided that a complete elimination of selected inflammatory mediators is rather detrimental as shown by the attenuation of neurological recovery. However, there are conflicting results reported on this issue which strongly depend on the experimental setting used. The history of immunoactivation in neurotrauma is the subject of this review article, giving particular emphasis to the comparison of clinical versus experimental studies performed over the last 10 years. These results also are evaluated with respect to other neuropathologies, which are years ahead as compared to the research in TBI. The possible reciprocal influence of peripheral and intrathecal activation of the immune system will also be discussed. To conclude, the future directions of research in the field of neurotrauma is considered.

Regulation of chemokines and chemokine receptors after experimental closed head injury.

The expression of the chemokines macrophage inflammatory protein (MIP)-2 and MIP-1alpha and of their receptors CXCR2 and CCR5 was assessed in wild type (WT) and TNF/lymphotoxin-alpha knockout (TNF/LT-alpha-/-) mice subjected to closed head injury (CHI). At 4 h after trauma intracerebral MIP-2 and MIP-1alpha levels were increased in both groups with MIP-2 concentrations being significantly higher in WT than in TNF/LT-alpha-/- animals (p < 0.05). Thereafter, MIP-2 production declined rapidly, whereas MIP-1alpha remained elevated for 7 days. Expression of CXCR2 was confined to astrocytes and increased dramatically within 24 h in both mouse types. Contrarily, CCR5 expression remained constitutively low and was mainly localized to microglia. These results show that after CHI, chemokines and their receptors are regulated differentially and with independent kinetics.

S-100 beta reflects the extent of injury and outcome, whereas neuronal specific enolase is a better indicator of neuroinflammation in patients with severe traumatic brain injury.

It has been hypothesized that immunoactivation may contribute to brain damage and affect outcome after traumatic brain injury (TBI). In order to determine the role of inflammation after TBI, we studied the interrelationship of the immune mediators sICAM-1 and IL-6 with the levels of S-100beta and neuronal specific enolase (NSE), both recognized markers of brain damage. In addition, the extent and type of cerebral injury and the neurological outcome were related to these measured markers of injury. An evident elevation of S-100beta (range of means: 2.7-81.4 ng/mL) and NSE (range of means: 2.0-81.3 ng/mL) was observed in CSF of all 13 patients during the first 3 posttraumatic days and decreased over 2 weeks. In parallel, the production of sICAM-1 (range of means: 0.7-11.9 ng/mL) and IL-6 (range of means: 0.1-8.2 ng/mL) was also markedly enhanced in CSF. The CSF means of S-100beta and NSE per patient correlated with IL-6 (r = 0.60, p < 0.05; and r = 0.64, p < 0.05, respectively), whereas the corresponding means in serum showed a significant correlation only between NSE and IL-6 (r = 0.56, p < 0.05). Maximal CSF values of NSE and sICAM-1 correlated with each other (r = 0.57, p < 0.05). The contusion sizes assessed on the CT scans correlated with the means of S-100beta (r = 0.63, p < 0.05) and NSE (r = 0.71, p < 0.05) in CSF and with the mean of S-100beta in serum, although not statistically significant (r = 0.52, p = 0.06), but not with serum NSE. Interestingly, linear regression analysis demonstrated that means of S-100beta in CSF (r = 0.78, p = 0.002) and serum (r = 0.82, p < 0.001) correlated with the GOS. These results indicate that the elevation of these parameters in CSF depends on the extent of injury and that S-100beta may be a predictor of outcome after TBI, whereas NSE reflects better the inflammatory response.

Upregulation of ICAM-1 and MCP-1 but not of MIP-2 and sensorimotor deficit in response to traumatic axonal injury in rats.

The pathophysiology of traumatic axonal injury (TAI) is only partially understood. In this study, we investigated the inflammatory response as well as the extent of neurological deficit in a rat model of traumatic brain injury (TBI). Forty-two adult rats were subjected to moderate impact-acceleration brain injury and their brains were analyzed immunohistochemically for ICAM-1 expression and neutrophil infiltration from 1 hr up to 14 days after trauma. In addition, the chemotactic factors MIP-2 and MCP-1 were measured in brain homogenates by ELISA. For evaluating the neurological deficit, three sensorimotor tests were applied for the first time in this model. In the first 24 hr after trauma, the number of ICAM-1 positive vessels increased up to 4-fold in cortical and subcortical regions compared with sham operated controls (P < 0.05). Maximal ICAM-1 expression (up to 8-fold increase) was detected after 4 days (P < 0.001 vs. 24 hr), returning to control levels in all brain regions by 7 days after trauma. MCP-1 was elevated between 4 hr and 16 hr post-injury as compared with controls. In contrast, neither neutrophil infiltration nor elevation of MIP-2, both events relevant in focal brain injury, could be detected. In all neurological tests, a significant deficit was observed in traumatized rats as compared with sham operated animals from Day 1 post-injury (grasping reflex of the hindpaws: P < 0.001, vibrissae-evoked forelimb placing: P = 0.002, lateral stepping: P = 0.037). In conclusion, after moderate impact acceleration brain injury ICAM-1 upregulation has been demonstrated in the absence of neutrophil infiltration and is paralleled by a selective induction of chemokines, pointing out that individual and distinct inflammatory events occur after diffuse vs. focal TBI.