Magneto-transport through graphene nano-ribbons

We investigate magneto-transport through graphene nano-ribbons as a function of gate and bias voltage, and temperature. We find that a magnetic field systematically leads to an increase of the conductance on a scale of a few tesla. This phenomenon is accompanied by a decrease in the energy scales associated to charging effects, and to hopping processes probed by temperature-dependent measurements. All the observations can be interpreted consistently in terms of strong-localization effects caused by the large disorder present, and exclude that the insulating state observed in nano-ribbons can be explained solely in terms of a true gap between valence and conduction band.Comment: 4 pages, 5 figure

Transport through Graphene on SrTiO₃

We report transport measurements through graphene on SrTiO3 substrates as a function of magnetic field B, carrier density n, and temperature T. The large dielectric constant of SrTiO3 very effectively screens long-range electron-electron interactions and potential fluctuations, making Dirac electrons in graphene virtually noninteracting. The absence of interactions results in an unexpected behavior of the longitudinal resistance in the N=0 Landau level and in a large suppression of the transport gap in nanoribbons. The “bulk” transport properties of graphene at B=0  T, on the contrary, are completely unaffected by the substrate dielectric constant

Role of metastasis-associated lung adenocarcinoma transcript-1 (MALAT-1) in pancreatic cancer - Fig 6

<p><b>(A) Fold-change in MALAT-1 gene expression in knockout mice as compared to the wild type.</b> (B) Sp1, Sp3, Sp4 and c-Myc expression in homozygous floxed p53/Kras^GD12 mice. (C) Survival of homozygous floxed p53L/L: Kras^GD12:p48Cre+/- mice expression MALAT-1 (+) or with loss of MALAT-1 (-/+). (D) Survival of heterozygous floxed p53L/+: Kras^GD12:p48Cre+/- mice expression MALAT-1 (+) or with loss of MALAT-1 (-/+). (E) Histology analysis of tumor samples from different strains of mice; images were 200X and 600X (for corner inserts). p-Values for significant differences in (C) and (D) were 0.39 and 0.26, respectively.</p

Role of metastasis-associated lung adenocarcinoma transcript-1 (MALAT-1) in pancreatic cancer - Fig 5

<p><b>(A) The structure of CDDO-Me and CF</b>_<b>3</b><b>DODA-Me.</b> Panc1 cells were treated with different concentrations of CDDO-Me or in combination of GSH, CF₃DODA-Me or in combination with GSH, and the changes of different proteins (B) and MALAT-1 expression (C) were determined by western blot and real time PCR, respectively. (D) Panc1 cells were transfected with siSp1/3/4 or siCtrl, and the MALAT-1 RNA expression was determined by real time PCR. Significant (p<0.05) changes are indicated (*) or (**).</p

Effects of MALAT-1 in pancreatic cell proliferation, cell cycle, apoptosis, migration and invasion.

<p>(A) MALAT-1 knockdown by RNAi in Panc1, MiaPaCa2 inhibited cell growth. (B) The effect of siMALAT-1 (knockdown) on cell cycle progression in Panc1 and MiaPaCa2 cells was determined by FACS analysis. (C) The apoptotic cells were quantified using FACS analysis and induction of PARP cleavage was determined by western blot analysis. MALAT-1 knockdown reduced cell migration (D) and cell invasion (E) as determined by scratch assay and Boyden chamber assay, respectively. Significant (p<0.05) changes are indicated (*).</p

Gene regulation by MALAT-1.

<p>(A) Panc1 cells were transfected with oligonucleotides (siMALAT-1#1/siMALAT-1#2) and expression of MALAT-1 was determined by real time PCR. (B) Panc1 cells were transfected with siMALAT-1 or siCtrl and gene expression was analyzed using Human HT-12 v4 expression beadchip (Illumina, Inc.) array. (C) The effects of siMALAT-1 on different function categories and the predicted activation state of cell proliferation, death and movement after HOTTIP knockdown were determined by IPA. (D) Pathway analysis. Causal IPA was used to analyze the p-values and Z-scores for cell movement proliferation and cell death after MALAT-1 knockdown by RNA interference.</p

Panc1 cells were transfected with siHOTTIP, siHOTAIR or siMALAT-1, and changes in gene expression were determined using human HT-12 V4 expression bead chip arrays.

<p>The overlap of total genes (A), proliferation inhibition (B), cell death (C) and inhibition of migration/invasion (D) genes coregulated by HOTTIP/HOTAIR, HOTTIP/MALAT-1 and HOTAIR/MALAT-1 was determined by IPA.</p