Thick branes with inner structure in mimetic f(R)f(R) gravity

In this paper, we study the structure and gravitational resonances of thick branes generated by a mimetic scalar field in $f(R)$ gravity. We obtain several typical thick brane solutions for $f(R)=R+\alpha R^2$. To study their stability, we analyze the tensor perturbation of the metric. It is shown that any thick brane model with $df/dR>0$ is stable and the graviton zero mode can be localized on the brane for each solution, which indicates that the four-dimensional Newtonian gravity can be restored. The effect of the parameter $\alpha$ on the gravitational resonances is studied. As a brane splits into multi sub-branes, the effective potential of the tensor perturbation will have an abundant inner structure with multi-wells, and this will lead to new phenomena of the gravitational resonances.Comment: 14 pages, 26 figures, improved version, references adde

Microglia in the aging brain: relevance to neurodegeneration

Microglia cells are the brain counterpart of macrophages and function as the first defense in the brain. Although they are neuroprotective in the young brain, microglia cells may be primed to react abnormally to stimuli in the aged brain and to become neurotoxic and destructive during neurodegeneration. Aging-induced immune senescence occurs in the brain as age-associated microglia senescence, which renders microglia to function abnormally and may eventually promote neurodegeneration. Microglia senescence is manifested by both morphological changes and alterations in immunophenotypic expression and inflammatory profile. These changes are likely caused by microinvironmental factors, but intrinsic factors cannot yet be completely excluded. Microglia senescence appears to underlie the switching of microglia from neuroprotective in the young brain to neurotoxic in the aged brain. The hypothesis of microglia senescence during aging offers a novel perspective on their roles in aging-related neurodegeneration. In Parkinson's disease and Alzheimer's disease, over-activation of microglia may play an active role in the pathogenesis because microglia senescence primes them to be neurotoxic during the development of the diseases

Car seat and occupant modelling using CAD

A current Brite-Euram project is concerned with life-cycle aspects of car seating with Loughborough being responsible for driver comfort assessment. This is being carried out through road and laboratory trials, with the results to be incorporated within the SAMMIE design system. Driver comfort is in part determined by seat pressure distributions which lead to deformation of the human flesh and the seat and movement of important design locations such as the driver's eyepoint. Accommodation of these effects requires a more realistic representation of the human body using surface rather than solid representations. Hence a shadow scanning technique is used to capture human body shape which is processed into the DUCT surface modelling system and via IGES files into SAMMIE. Finite element techniques are then used to predict deformations at the seat/driver interface

Inhibition of LY294002 in retinal neovascularization via down-regulation the PI3K/AKT-VEGF pathway in vivo and in vitro

AIM: To investigate the effects of the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 on retinal neovascularization (RNV) in the oxygen-induced retinopathy (OIR) mouse model and human umbilical vein endothelial cells (HUVECs). METHODS: C57BL/6J mice were randomly divided into normoxia-control, OIR-control and LY294002 treatment groups. LY294002 or phosphate-buffered solution was intraperitoneally injected daily into mouse pups from P6 to P9 in LY294002 treatment group or OIR-control group. Morphological and pathological changes in RNV, as well as expression levels of PI3K, serine-threonine kinase (AKT) and vascular endothelial growth factor (VEGF) were observed. HUVECs treating with LY294002 were exposed to hypoxia; the expression of PI3K, AKT and VEGF were examined by Western blot and RT-PCR analyses. RESULTS: Compared with the OIR-control group, LY294002 significantly inhibit RNV. Adenosine diphosphatase (ADPase) staining and hematoxylin and eosin staining indicated that the clock hour scores of neovascularization and the nuclei of pre-retinal neovascular cells in the LY294002 treatment group were clearly less than those in the OIR-control group (1.41±0.52 vs 6.20±1.21; 10.50±1.58 vs 22.25±1.82, both P<0.05). Intravitreal injection of LY294002 (in the LY294002 treatment group) markedly decreased PI3K/AKT-VEGF expression compared with the OIR-control group by immunohistochemistry, Western blotting and RT-PCR (all P<0.05). In HUVECs treated with hypoxia, expression of PI3K, AKT and VEGF were downregulated in the hypoxia-LY294002 group (all P<0.05). CONCLUSION: The PI3K inhibitor LY294002 can inhibit RNV by downregulating PI3K, AKT, and VEGF expression in vivo and in vitro. LY294002 may provide an effective method for preventing retinopathy of prematurity (ROP)