Fano Scattering: Manifestation of Acoustic Phonons at the Nanoscale

Size-dependent asymmetric low-frequency Raman line shapes have been observed from silicon (Si) nanostructures (NSs) due to a quantum confinement effect. The acoustic phonons in Si NSs interact with an intraband quasi-continuum to give rise to Fano interaction in the low-frequency range. The experimental asymmetric Raman line shape has been explained by developing a theoretical model that incorporates the quantum-confined phonons interacting with an intraband quasi-continuum available in Si NSs as a result of discretization of energy levels with unequal separation. We discover that a phenomenon similar to Brillouin scattering is possible at the nanoscale in the low-frequency regime and thus may be called “Fano scattering” in general. A method has been proposed to extract information about nonradiative transitions from the Fano scattering data where these nonradiative transitions are involved as an intraband quasi-continuum in modulation with discrete acoustic phonons

TEM micrograph of magnetic nano particles.

<p>The average particle size is ∼ 60 nm.</p

MNP bound BDNF efficiently crosses BBB and induces CREB expression.

<p>Free and bound BDNF were added to the respective wells of BBB, in the upper chamber. A weak magnet was placed on the basal side of BBB. Astrocytes (3X10⁶/ml) were collected from basal side, RNA was extracted, reverse transcribed, cDNA amplified, and gene expression of CREB was determined by real-time quantitative PCR. These data are the mean ± SD of 3 separate experiments.</p

Binding isotherm for BDNF on MNP.

<p>Ratios of 1∶0.05, 1∶0.01, 1∶0.015, 1∶0.02, 1∶0.025, 1∶0.03, 1∶0.35 of MNP and BDNF were used for 3 hrs. Binding efficiency (µg BDNF/mg MNP) was calculated by ELISA.</p

Morphine induced spine density is reversed by MNP bound BDNF.

<p>(A) Spine density measurement by Image J analysis. SK-N-MC neuroblastoma cells were grown onto glass coverslips placed in a petridish and treated with BDNF and/or morphine. After treatment, cells were stained with 1, 1′-Dioctadecyl-3, 3,3′,3′-tetramethylindocarbocyanine perchlorate (DiI) and visualized using confocal microscope. Representative image is shown in fig. 7A. (B) Dendritic segments were chosen randomly from the apical and basal regions. The length of randomly selected dendritic segment was measured, the number of spines along that length was counted and spine density was calculated by dividing the total number of spines by dendrite length, as expressed as spines/µm. Figure represents mean of 3 different experiments.</p

Transendothelial electrical resistance (TEER) values before and after treatment with MNP-BDNF.

<p>Transendothelial electrical resistance (TEER) values before and after treatment with MNP-BDNF.</p

MNP bound BDNF is effective in suppressing the apoptosis induced by morphine.

<p>(A) Morphine induces apoptosis of human PBMCs. PBMCs were cultured alone or with 10⁻⁷ M concentration of morphine for 48 hrs. Free and bound BDNF (10, 50,100 ng/ml) were added to respective cultures 24 hr before morphine treatment. After treatment, cells are stained with Annexin-V and 7-AAD analyzed by FACScalibur within 1 hr. The untreated cells, which served as control, is used for defining the basal level of apoptotic and dead cells. (B) Representative histogram showing Annexin-V expression in treated cells.</p

MNP is not toxic to the PBMC.

<p>PBMC (1X10⁶/ml) treated with free and bound BDNF were stained with live-dead cell discrimination dye ViViD and analyzed by flowcytometry.</p

MNP bound BDNF reverses morphine induced CREB downredulation in astrocytes.

<p>(A) Morphine significantly downregulated CREB gene expression. Astrocytes (1X10⁶/ml) were cultured with or without morphine (10⁻⁷ M) for 48 hrs; RNA was extracted, reverse transcribed, cDNA amplified, and gene expression of CREB was determined by real-time quantitative PCR. These data are the mean ± SD of 3 separate experiments. (B) Astrocytes (3X10⁶/ml) were cultured with free and bound BDNF 24 hr before morphine (10⁻⁷ M) treatment. RNA was extracted, reverse transcribed, cDNA amplified, and gene expression of CREB was determined by real-time quantitative PCR. These data are the mean ± SD of 3 separate experiments.</p

HIV replication increased in MDDCs treated with cocaine.

<p><b>(A)</b> MDDCs (1×10⁶ cells/ml) from normal donors were infected with HIV-1_BAL at a concentration of 20 ng for 2 hr, followed by treatment ± cocaine (1 µM) for 7 days. The culture supernatants were quantitated for p24 Ag. Significance is calculated with respect to HIV-1 treated control cells. (<b>B</b>) Effect of cocaine on HIV-1 transcription was determined using an LTR-CAT reporter data normalized to total protein concentration. (<b>C</b>) HIV-1 transcription was determined in MDDCs from normal donors infected with HIV-luciferase viruses competent for a single round of infection (∼20 ng per (1×10⁶ cells) in the presence/absence of cocaine (1 µM) for 72 hours. Cultures were harvested 72 hours post infection and luciferase assayed. Results shown are representative of mean ± SEM of three experiments. p-value≤0.05 were considered to be significant.</p