Functionalization of graphenic surfaces by oxygen plasma toward enhanced wettability and cell adhesion : experiments corroborated by molecular modelling

Graphenic materials attract huge attention because of their outstanding properties, and have a wide range of applications as, i.e., components of biomaterials. Due to their hydrophobic nature, however, the surfaces need to be functionalized to improve wettability and biocompatibility. In this study, we investigate the functionalization of graphenic surfaces by oxygen plasma treatment, introducing surface functional groups in a controlled way. The AFM images and LDI-MS results clearly show that the graphenic surface exposed to plasma is decorated with -OH groups, whereas the surface topography remains intact. The measured water contact angle decreases significantly after oxygen plasma treatment from $99^{\circ}$ to ca. $5^{\circ}$, making the surface hydrophilic. It is also reflected in the surface free energy values which increase from 48.18 mJ $m^{−2}$ to 74.53 mJ $m^{−2}$ when the number of surface oxygen groups reaches 4 -OH/84 $Å^{2}$. The DFT (VASP) molecular models of unmodified and oxygen-functionalized graphenic surfaces were constructed and used for molecular interpretation of water-graphenic surface interactions. The computational models were validated by comparison of the theoretically determined water contact angle (based on the Young–Dupré equation) to the experimentally determined values. Additionally, the VASPsol (implicit water environment) results were calibrated against the explicit water models that can be used in further research. Finally, the biological role of functional groups on the graphenic surface was examined in terms of cell adhesion with the use of mouse fibroblast cell line (NIH/3T3). The obtained results illustrate the correlation between surface oxygen groups, wettability, and biocompatibility providing the guidelines for the molecular level-driven design of carbon materials for various applications

Glucocorticoid-regulated kinase CAMKIγ\gamma in the central amygdala controls anxiety-like behavior in mice

The expression of the Calcium/Calmodulin-Dependent Protein Kinase I gamma (encoded by the Camk1g gene) depends on the activation of glucocorticoid receptors (GR) and is strongly regulated by stress. Since Camk1g is primarily expressed in neuronal cells of the limbic system in the brain, we hypothesized that it could be involved in signaling mechanisms that underlie the adaptive or maladaptive responses to stress. Here, we find that restraint-induced stress and the GR agonist dexamethasone robustly increase the expression of Camk1g in neurons of the amygdalar nuclei in the mouse brain. To assess the functional role of Camk1g expression, we performed a virally induced knock-down of the transcript. Mice with bilateral amygdala-specific Camk1g knock-down showed increased anxiety-like behaviors in the light-dark box, and an increase in freezing behavior after fear-conditioning, but normal spatial working memory during exploration of a Y-maze. Thus, we confirm that Camk1g is a neuron-specific GR-regulated transcript, and show that it is specifically involved in behaviors related to anxiety, as well as responses conditioned by aversive stimuli

Mechanisms of attenuation of pulmonary V'O_{2} slow component in humans after prolonged endurance training

In this study we have examined the effect of prolonged endurance training program on the pulmonary oxygen uptake (V'O2 ) kinetics during heavy-intensity cycling-exercise and its impact on maximal cycling and running performance. Twelve healthy, physically active men (mean\ub1SD: age 22.33\ub11.44 years, V'O2peak 3198\ub1458 mL \ub7 min-1 ) performed an endurance training composed mainly of moderate-intensity cycling, lasting 20 weeks. Training resulted in a decrease (by 3c5%, P = 0.027) in V'O2 during prior low-intensity exercise (20 W) and in shortening of \u3c4 p of the V'O2 on-kinetics (30.1\ub15.9 s vs. 25.4\ub11.5 s, P = 0.007) during subsequent heavy-intensity cycling. This was accompanied by a decrease of the slow component of V'O2 on-kinetics by 49% (P = 0.001) and a decrease in the end-exercise V'O2 by 3c5% (P = 0.005). An increase (P = 0.02) in the vascular endothelial growth factor receptor 2 mRNA level and a tendency (P = 0.06) to higher capillary-to-fiber ratio in the vastus lateralis muscle were found after training (n = 11). No significant effect of training on the V'O2peak was found (P = 0.12). However, the power output reached at the lactate threshold increased by 19% (P = 0.01). The power output obtained at the V'O2peak increased by 14% (P = 0.003) and the time of 1,500-m performance decreased by 5% (P = 0.001). Computer modeling of the skeletal muscle bioenergetic system suggests that the training-induced decrease in the slow component of V'O2 on-kinetics found in the present study is mainly caused by two factors: an intensification of the each-step activation (ESA) of oxidative phosphorylation (OXPHOS) complexes after training and decrease in the "additional" ATP usage rising gradually during heavy-intensity exercise

Genotype-dependent consequences of traumatic stress in four inbred mouse strains

Post-traumatic stress disorder (PTSD) is an anxiety disorder that develops in predisposed individuals following a terrifying event. Studies on isogenic animal populations might explain susceptibility to PTSD by revealing associations between the molecular and behavioural consequences of traumatic stress. Our study employed four inbred mouse strains to search for differences in post-stress response to a 1.5-mA electric foot shock. One day to 6 weeks after the foot shock anxiety, depression and addiction-like phenotypes were assessed. In addition, expression levels of selected stress-related genes were analysed in hippocampus and amygdala. C57BL/6J mice exhibited up-regulation in the expression of Tsc22d3, Nfkbia, Plat and Crhr1 genes in both brain regions. These alterations were associated with an increase of sensitized fear and depressive-like behaviour over time. Traumatic stress induced expression of Tsc22d3, Nfkbia, Plat and Fkbp5 genes and developed social withdrawal in DBA/2J mice. In 129P3/J strain, exposure to stress produced the up-regulation of Tsc22d3 and Nfkbia genes and enhanced sensitivity to the rewarding properties of morphine. Whereas, SWR/J mice displayed increase only in Pdyn expression in the amygdala and had the lowest conditioned fear. Our results reveal a complex genetic background of phenotypic variation in response to stress and indicate the SWR/J strain as a valuable model of stress resistance. We found potential links between the alterations in expression of Tsc22d3, Nfkbia and Pdyn, and different aspects of susceptibility to stress

Engineering of bone fixation metal implants biointerface : application of parylene C as versatile protective coating

The tribological and protective properties of parylene C coatings (2 – 20 μ m) on stainless steel 316L implant materials were investigated by means of electrochemical measurements and wear tests. The thickness and morphology of the CVD prepared coatings were characterized by scanning electron and laser confocal mi- croscopy. The stability of the coatings was examined in contact with Hanks' solution and H 2 O 2 (simulating the in fl ammatory response). It was concluded that silane – parylene C coating with the optimum thickness of 8 μ m exhibits excellent wear resistance properties and limits the wear formation. The engineered versatile coating demonstrates suf fi cient elastomer properties, essential to sustain the implantation surgery strains and micromotions during long-term usage in the body