Status epilepticus increases brain-blood barrier (BBB) permeability leading to vasogenic edema. This BBB disruption is usually confined within relatively limited cerebral regions including the piriform cortex (PC), and leads to epileptogenesis and contributes to progression of epilepsy. Although cytokines are at least partly responsible for changes in BBB permeability, the role of interleukin-18 (IL-18) in vasogenic edema is not yet explored in detail. In the present study, we investigated the role of IL-18 in SE-induced vasogenic edema formation. Following SE, IL-18/interferon-γ (IFN-γ) system was up-regulated in astrocytes and microglia/macrophages. Recombinant rat (rr) IL-18 infusion decreased vasogenic edema formation, while anti-rat IL-18 infusion increased it. In contrast, rrIFN-γ, and anti-rat IFN-γ infusion showed reverse effects on vasogenic edema formation. rrIL-18 or anti-rat IFN-γ IgG infusion elevated dystrophin expression accompanied by the reduction in vasogenic edema. However, rr-IFN-γ or anti-rat IL-18 IgG infusion significantly decreased dystrophin immunoreactivity within the PC following SE. These findings indicate that IL-18-mediated up-regulation of dystrophin expression may play either a direct or indirect role in maintenance of BBB function following SE. Therefore, our findings suggest that IL-18 may have protective effect on SE-induced BBB disruption in IFN-γ independent mechanism.

Recently, we have reported that astroglial activations in response to status epilepticus (SE) show regional-specific manners in the rat hippocampus. However, it is unknown that microglial responses to SE would show regional-specific patterns. Therefore, the present study was designed to elucidate the regional-specific microglial activation and relationship between P2X7 receptor functions and SE-induced microglial responses in the rat brain. Following SE, microglia appeared amoeboid or phagocytic in the dentate gyrus and the piriform cortex. In contrast, elongated microglia were observed in the CA1 hippocampal regions and the frontoparietal cortex. In the dentate gyrus, the CA1 hippocampal regions, and the frontoparietal cortex, these microglial activation accelerated by BzATP (a P2X7 receptor agonist)-infusion, but inhibited by OxATP (a P2X7 receptor antagonist). However, SE-induced microglial activation in the piriform cortex was not affected by BzATP or OxATP-infusion. Therefore, our findings indicate that SE-induced microglial activation may show regional-specific manners, and suggest that P2X7 receptor function differently modulates SE-induced microglial responses in distinct brain regions.

Endothelin-1 (ET-1) is one of potential factors to induce vasogenic edema formation, since exogenous ET-1 treatment decreases aquaporin 4 (AQP4) expression and increases chemokines induction. To identify the role of endogenous ET-1 in vasogenic edema formation, we examined the correlation between endogenous ET-1 expression and vasogenic edema formation in the pirifom cortex following status epilepticus (SE). In the present study, SMI-71 (a brain-blood barrier marker) immunoreactivity was significantly reduced in blood vessels at 1 day after SE when vasogenic edema and neuronal damage were observed. ET-1 expression was up-regulated in endothelial cells prior to reduction in SMI-71 immunoreactivity. Furthermore, ET-1 expressing endothelial cells showed the absence of SMI-71 immunoreactivity. Increase in ET-1 expression was followed by reduced AQP4 immunoreactivity prior to vasogenic edema formation. Only a few microglia showed monocyte chemotactic protein-1 (a chemokine induced by ET-1) outside vasogenic edema lesion. Taken together, our findings suggest that endothelial ET-1 expression may contribute to SE-induced vasogenic edema formation via brain-blood barrier disruption at AQP4/MCP-1 independent manners.

We report a simple method to prepare hierarchically structured TiO(2) spheres (HS-TiO(2)), using an electrostatic spray technique, that are utilized for photoelectrodes of highly efficient dye-sensitized solar cells (DSSCs). This method has an advantage to remove the synthesis steps in conventional sol-gel method to form nano-sized spheres of TiO(2) nanoclusters. The fine dispersion of commercially available nanocrystalline TiO(2) particles (P25, Degussa) in EtOH without surfactants and additives is electro-sprayed directly onto a fluorine-dopoed tin-oxide (FTO) substrate for DSSC photoelectrodes. The DSSCs of HS-TiO(2) photoelectrodes show high energy conversion efficiency over 10% under illumination of light at 100 mW cm(-2), AM1.5 global. It is concluded from frequency-dependent measurements that the faster electron diffusion coefficient and longer lifetime of HS-TiO(2) than those in nonstructured TiO(2) contribute to the enhanced efficiency in DSSCs.

Although nuclear factor-kappa B (NF-κB) is essential for neuron survival and its activation may protect neuron against oxidative-stresses or ischemia-induced neurodegeneration, NF-κB activation can contribute to inflammatory reaction and apoptotic cell death after brain injury and stroke. However, there are little data concerning the specific pattern of NF-κB phosphorylations in neuronal damage/survival induced by status epilepticus (SE). In the present study, NF-κB phosphorylation showed the cellular specific pattern in responses to SE. p52-S865, p52-Ser869, p65-Ser276, p65-Ser311, p65-Ser468, and p65-Ser529 NF-κB phosphorylation was significantly decreased in the CA1 and CA3 pyramidal cells vulnerable to SE, although neuronal specific nuclear antigen immunoreactivity was strongly detected. In contrast, p65-Ser536 NF-κB phosphorylation was enhanced in these neurons accompanied by TUNEL- and Fluoro-Jade B 244signals. These findings serve as the first comprehensive description of the cellular specific distribution of NF-κB phosphorylation in response to pilocarpine-induced SE in the rat hippocampus, and suggest that enhancement in p65-Ser536 NF-κB phosphorylation may be closely relevant to neuronal vulnerability to SE, while others may be involved in neuronal survival.

Niemann-Pick type C disease (NPC) is an autosomal recessive disorder that results in premature death due to progressive neurodegeneration including dementia. To understand neuronal pathways connecting to the hippocampus, retrograde transneuronal labeling method with Bartha strain of pseudorabies virus (PRV) was employed in 40 NPC+/+, NPC+/- and NPC-/- mice. Immunohistochemistry using polyclonal antibody against PRV and streological counting were used. The number of neurons and synapse in CA2&3 regions of the hippocampus decreased dramatically in the NPC-/- mouse compared to the NPC+/+ or +/- mouse. The number of PRV positive cell was significantly decreased in several regions including the entorhinal and piriform cortex in the NPC-/- mouse. More severely, lateral septal dorsal nucleus, dorsal entorhinal cortex and medial geniculate body showed no positive labeling in the NPC-/- mouse. However, the hippocampus, medial septal and supramammilary nuclei showed increased immunoreactivity in the NPC-/- mouse. Our data suggest that the synaptic loss and discontinuity of the CNS hippocampal pathway may contribute to understanding the mechanism of symptoms and functional disabilities such as memory and learning disturbance in NPC patients.

Submicroscale SiC fiber mats were prepared by the electrospinning of an oil-in-water(O/W) precursor emulsion, a subsequent thermal curing treatment, and calcination at 1600 °C. Low-molecular-weight PCS micelles entrapped within an aqueous PVP matrix played an important role in forming the continuous and dense core structure, resulting in pure SiC fibers. The manipulation of SiC fiber diameters could be obtained via control of the micellar PCS concentration (10-30 wt %), enabling the production of dense and highly crystallized SiC fiber architectures with diameters ranging from 200 to 350 nm.

High-performance, room-temperature (RT), solid-state dye-sensitized solar cells (DSSCs) were fabricated using hierarchically structured TiO₂ nanofiber (HS-NF) electrodes and plastic crystal (PC)-based solid-state electrolytes. The electrospun HS-NF photoelectrodes possessed a unique morphology in which submicrometer-scale core fibers are interconnected and the nanorods are dendrited onto the fibers. This nanorod-in-nanofiber morphology yielded porosity at both the mesopore and macropore level. The macropores, steming from the interfiber space, afforded high pore volumes to facilitate the infiltration of the PC electrolytes, whereas the mesoporous nanorod dendrites offered high surface area for enhanced dye loading. The solid-state DSSCs using HS-NFs (DSSC-NF) demonstrated improved power conversion efficiency (PCE) compared to conventional TiO₂ nanoparticle (NP) based DSSCs (DSSC-NP). The improved performance (>2-fold) of the DSSC-NFs was due to the reduced internal series resistance (R(s)) and the enhanced charge recombination lifetime (τ(r)) determined by electrochemical impedance spectroscopy and intensity modulated photocurrent/photovoltage spectroscopy. The easy penetration of the PC electrolytes into HS-NF layers via the macropores reduces R(s) significantly, improving the fill factor (FF) of the resulting DSSC-NFs. The τ(r) difference between the DSSC-NF and DSSC-NP in the PC electrolytes was extraordinary (~14 times) compared to reported results in conventional organic liquid electrolytes. The optimized PCE of DSSC-NF using the PC electrolytes was 6.54, 7.69, and 7.93% at the light intensity of 100, 50, and 30 mW cm⁻², respectively, with increased charge collection efficiency (>40%). This is the best performing RT solid-state DSSC using a PC electrolyte. Considering the fact that most reported quasi-solid state or nonvolatile electrolytes require higher iodine contents for efficient ion transport, our HS-NFs are a promising morphology for such electrolytes that have limited ion mass transport.

In the present study we analyzed aquaporin-4 (AQP4) immunoreactivity in the piriform cortex (PC) and the hippocampus of pilocarpine-induced rat epilepsy model to elucidate the roles of AQP4 in brain edema following status epilepticus (SE). In non-SE-induced animals, AQP4 immunoreactivity was diffusely detected in the PC and the hippocampus. AQP4 immunoreactivity was mainly observed in the endfeet of astrocytes. Following SE the AQP4-deleted area was clearly detected in the PC, not in the hippocampus. Decreases in dystrophin and α-syntrophin immunoreactivities were followed by reduction in AQP4 immunoreactivity. These alterations were accompanied by the development of vasogenic edema and the astroglial loss in the PC. In addition, acetazolamide (an AQP4 inhibitor) treatment exacerbated vasogenic edema and astroglial loss both in the PC and in the hippocampus. These findings suggest that SE may induce impairments of astroglial AQP4 functions via disruption of the dystrophin/α-syntrophin complex that worsen vasogenic edema. Subsequently, vasogenic edema results in extensive astroglial loss that may aggravate vasogenic edema.

Water-soluble, polyelectrolyte-grafted multiwalled carbon nanotubes (MWCNTs), MWCNT-g-PSSNa, were synthesized using a "grafting to" route. MWCNT-g-PSSNa thin films fabricated by an electrostatic spray (e-spray) technique were used as the counter electrode (CE) for dye-sensitized solar cells (DSSCs). The e-sprayed MWCNT-g-PSSNa thin-film-based CEs (MWCNT-CE) were uniform over a large area, and the well-exfoliated MWCNTs formed highly interconnected network structures. The electrochemical catalytic activity of the MWCNT-CE at different thicknesses was investigated. The MWCNT-g-PSSNa thin film showed high efficiency as a CE in DSSCs. The power conversion efficiency (PCE) of the DSSCs using the MWCNT-g-PSSNa thin-film-based CE (DSSC-MWCNT) was >6% at a CE film thickness of approximately 0.3 microm. The optimum PCE was >7% at a film thickness of approximately 1 microm, which is 20-50 times thinner than conventional carbon-based CE. The charge transfer resistance at the MWCNT-CE/electrolyte interface was 1.52 Omega cm(2) at a MWCNT-CE thickness of 0.31 microm, which is lower than that of a Pt-CE/electrolyte interface, 1.78 Omega cm(2). This highlights the potential for the low-cost CE fabrication of DSSCs using a facile deposition technique from an environmentally "friendly" solution at low temperatures.