Thermoelectric Properties of Thermally Reduced Graphene Oxide Observed by Tuning the Energy States

Reduced graphene oxide (rGO) possesses a similar electronic structure to graphene but can be synthesized on a larger scale. Hence, rGO is considered as an attractive alternative to graphene. Here we report the carrier transport properties of thermally reduced graphene oxide (TrGO) as a function of reduction temperature. The transfer curve of a field effect transistor fabricated with TrGO exhibited ambipolar properties, and the charge neutrality point of TrGO was shifted from negative to positive as the reduction temperature increased. Furthermore, as revealed in Arrhenius plots of the carrier densities and carrier mobilities, TrGO behaved as a metallic conductor at all reduction temperatures. To investigate the effect of reduction temperature on the thermoelectric properties of TrGO, the Seebeck coefficients of the fabricated TrGOs were calculated from the transfer curve using Mott’s equation for metallic materials. All samples showed ambipolar carrier transport. At <i>V</i>_g = 0 V, the Seebeck coefficient switched sign from negative to positive as the reduction temperature became higher, indicating that electron and hole carrier transport dominates at higher and lower reduction temperature, respectively. The calculated Seebeck coefficients at zero gate bias were compared with the measured coefficients in TrGO bulk films. The thermoelectric properties of the measured and calculated coefficients showed similar trends with increasing reduction temperature, and the charged carrier transport (i.e., the energy states) of TrGO can be tuned by varying the reduction temperature without doping with impurities

Amelioration of Huntington's disease phenotypes by Beta-Lapachone is associated with increases in Sirt1 expression, CREB phosphorylation and PGC-1α deacetylation

<div><p>Huntington’s disease (HD) is one of the most devastating genetic neurodegenerative disorders with no effective medical therapy. β-Lapachone (βL) is a natural compound obtained from the bark of the Lapacho tree and has been reported to have beneficial effects on various diseases. Sirt1 is a deacetylase of the sirtuin family and deacetylates proteins including the peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) which is associated with mitochondrial respiration and biogenesis. To examine the effectiveness of βL on HD, βL was orally applied to R6/2 HD mice and behavioral phenotypes associated with HD, such as impairment of rota-rod performance and increase of clasping behavior, as well as changes of Sirt1 expression, CREB phosphorylation and PGC-1α deacetylation were examined. Western blot results showed that Sirt1 and p-CREB levels were significantly increased in the brains of βL-treated R6/2 mice. An increase in deacetylation of PGC-1α, which is thought to increase its activity, was observed by oral administration of βL. In an <i>in vitro</i> HD model, βL treatment resulted in an attenuation of MitoSOX red fluorescence intensity, indicating an amelioration of mitochondrial reactive oxygen species by βL. Furthermore, improvements in the rota-rod performance and clasping score were observed in R6/2 HD mice after oral administration of βL compared to that of vehicle control-treated mice. Taken together, our data show that βL is a potential therapeutic candidate for the treatment of HD-associated phenotypes, and increases in Sirt1 level, CREB phosphorylation and PGC-103B1 deacetylation can be the possible underlying mechanism of the effects of βL.</p></div

Decrease in mitochondrial superoxide level by βL treatment of an <i>in vitro</i> HD model.

<p>R6/2 mouse-derived NSCs were cultured and differentiated in a differentiation medium. After differentiation, βL was added for 3 days and mitochondrial superoxide levels were measured by immunocytochemistry (A) and flow cytometry (B) after MitoSOX red staining. The red, roundish objects are individual cells with MitoSOX staining, and the M1 marker of the flow cytometry result indicats a Cy3-positive population. The percentage values of NSCs with M1 after vehicle or βL treatment are represented in a bar graph (n = 3) (C). The graph shows means ± SEM. *p < 0.05 indicates significant differences when compared to the vehicle-treated group.</p

Reduction in PGC-1α acetylation by βL administration in mice.

<p>βL was orally administered to R6/2 mice for 6 weeks from 5 to 11 weeks of age. After the sacrifice, brains were isolated and an immunoprecipitation was performed using the PGC-1α antibody. Immunoprecipitated proteins were separated by SDS-PAGE and blotted with anti-PGC-1α and anti-acetylated-lysine antibodies to measure the level of PGC-1α acetylation. Relative band intensities were analyzed using the Image J software. The acetylation level of PGC-1α was analyzed by the intensity of acetylated lysine relative to the amount of total PGC-1α (lower panel). The graph shows means ± SEM. *p < 0.01 indicates significant differences when compared to the control group.</p

Microstructure of Polycrystalline PBTTT Films: Domain Mapping and Structure Formation

We utilize near-edge X-ray absorption fine structure (NEXAFS) spectroscopy and scanning transmission X-ray microscopy (STXM) to study the microstructure and domain structure of polycrystalline films of the semiconducting polymer poly(2,5-bis(3-tetradecylthiophen-2-yl)thieno[3,2-<i>b</i>]thiophene) (PBTTT). Total electron yield NEXAFS spectroscopy is used to examine the surface structure of the first 1–2 molecular layers, while bulk-sensitive STXM is used to produce maps of domain orientation and order sampled through the entire film thickness. We study different phases of PBTTT including as-cast, terraced and nanoribbon morphologies produced <i>via</i> spin-coating as well as aligned films of as-cast and nanoribbon morphologies produced by zone-casting. For the terraced morphology, domains are observed that are larger than the size of the terraced surface features, and the calculated degree of order is reduced compared to the nanoribbon morphology. For zone-cast films, we find that, although little optical anisotropy is observed in the bulk of as-cast films, a high degree of surface structural anisotropy is observed with NEXAFS spectroscopy, similar to what is observed in annealed nanoribbon films. This observation indicates that the aligned surface structure in unannealed zone-cast films templates the bulk ordering of the aligned nanoribbon phase. STXM domain mapping of aligned nanoribbon films reveals elongated, micrometer-wide domains with each domain misoriented with respect to its neighbor by up to 45°, but with broad domain boundaries. Within each nanoribbon domain, a high degree of X-ray dichroism is observed, indicating correlated ordering throughout the bulk of the film

Cytosolic Extract of Human Adipose Stem Cells Reverses the Amyloid Beta-Induced Mitochondrial Apoptosis via P53/Foxo3a Pathway

<div><p>Human adipose stem cells (hASC) have therapeutic potential for the treatment of neurodegenerative disorders. Mitochondrial dysfunction is frequently observed in most neurodegenerative disorders, including Alzheimer’s disease. We explored the therapeutic potential of hASC cytosolic extracts to attenuate neuronal death induced by mitochondrial dysfunction in an Alzheimer’s disease (AD) <i>in vitro</i> models. Amyloid beta (Aβ) was used to induce cytotoxity in an immortal hippocampal cell line (HT22) and neuronal stem cells from the brain of TG2576 transgenic mice were also used to test the protective role of hASC cytosolic extracts. Cell viability and flow cytometry results demonstrated that the hASC extract prevents the toxicity and apoptosis in AD <i>in vitro</i> models. Moreover, JC-1 and MitoSoxRed staining followed by fluorescence microscopy and flow cytometry results showed that the hASC extract ameliorated the effect of Aβ-induced mitochondrial oxidative stress and reduced the mitochondrial membrane potential. Western blot result showed that hASC extract modulated mitochondria-associated proteins, such as Bax and Bcl2, and down-regulated cleaved caspase-3. In addition, hASC extract decreased Aβ generation and reversed up-regulated p53 and foxo3a protein level in AD <i>in vitro</i> model cell derived from TG2576 mice. Taken together, these findings implicate a protective role of the hASC extract in the Aβ-induced mitochondrial apoptosis via regulation of P53/foxo3a pathway, providing insight into the molecular mechanisms of hASC extract and a therapeutic strategy to ameliorate neuronal death induced by Aβ.</p></div

Striatal atrophy and mHtt aggregation.

<p>(A) Striatal mHtt aggregation was mitigated in ASCs-E treated group. (B) mHtt aggregation was visualized by western blot. (C) mHtt aggregation level was higher in ASCs-E treated R6/2 mouse brain compared with R6/2 control. (D) Striatum was sectioned and stained with Nissl in R6/2 mouse treated with ASCs-E or vehicle. (E) Striatum/peristriatum ratio is higher in ASCs-E injected group compared with vehicle treated group. Bar  = 100 μm, * <i>p</i><0.01.</p

The hASC extract prevents Aβ-induced cell toxicity.

<p>HT22 cells were treated with 100 μg/ml Aβ with or without 30 μg/ml of the hASC extract. At 48 h, (A) cells were directly imaged with a microscope. Representative images are shown. (B) The cell viability assay using CCK8 shows the reduction of cell viability by treatment with Aβ and the hASC extract; normalized values are presented (<i>n</i> = 3 each). (C, D) Cells were subjected to Annexin V-FITC and (or) PI staining. Images captured by a fluorescent microscope; or cells were analyzed using flow cytometry and quantified graph shows the level of apoptosis in the experiments (<i>n</i> = 3 each). Scale bar = 10 μm (A); 50 μm (C). Error bars represent S.E.M. *p<0.05, **p<0.01.</p

Experimental schedule and disease phenotypes of R6/2 mice.

<p>(A) Schedule for ASCs-E injection, behavior test, weight measure and brain sampling. (B) ASCs-E injection mitigated weight loss in R6/2 mouse at 12 weeks age. (C) Rotarod test showed better motor performance at 10, 11 and 12 weeks of age in ASCs-E treated R6/2 compared with control. * <i>p</i><0.05, ** <i>p</i><0.01.</p

The hASC extract prevents Aβ -induced mitochondrial dysfunction.

<p>HT22 cells were treated with 100 μg/ml Aβ with or without 30 μg/ml of the hASC extract at 24h after seeding. At 48 h, (A, B) cells were subjected to JC-1 staining. Data showed induction of the JC-1 monomer by Aβ treatment with the hASC extract reduced this effect (<i>n</i> = 3 each). (C) Cells were subjected to MitoSoxRed staining. MitoSoxRed intensity was decreased by Aβ but normalized by the hASC extract (<i>n</i> = 3 each). (D) HT22 cells were transfected with mito-dsRed with 100 μg/ml Aβ and 30 μg/ml hASC extract. The mitochondrial length was reduced by Aβ and this effect was normalized by treatment with the hASC extract (n = 3 each). At least 15 cells were selected in each sample and about 40 mitochondria were examined from each selected cell. Error bars represent S.E.M. Scale bar = 10 μm. **p<0.01, ***p<0.001.</p