Exciton dephasing and biexciton binding in CdSe/ZnSe islands

The dephasing of excitons and the formation of biexcitons in self-organized CdSe/ZnSe islands grown by molecular-beam epitaxy is investigated using spectrally resolved four-wave mixing. A distribution of exciton-exciton scattering efficiencies and dephasing times in the range of 0.5–10 ps are observed. This indicates the presence of differently localized exciton states at comparable transition energies. Polarization-dependent measurements identify the formation of biexcitons with a biexciton binding energy of more than four times the bulk value. With decreasing exciton energy, the binding energy slightly increases from 21.5 to 23 meV, while its broadening decreases from 5.5 to 3 meV. This is attributed to a strong three-dimensional confinement with improving shape uniformity for decreasing exciton energy

Excitons, biexcitons, and phonons in ultrathin CdSe/ZnSe quantum structures

The optical properties of CdSe nanostructures grown by migration-enhanced epitaxy of CdSe on ZnSe are studied by time-, energy-, and temperature-dependent photoluminescence and excitation spectroscopy, as well as by polarization-dependent four-wave mixing and two-photon absorption experiments. The nanostructures consist of a coherently strained Zn1−xCdxSe/ZnSe quantum well with embedded islands of higher Cd content with sizes of a few nanometer due to strain-induced CdSe accumulation. The local increase in CdSe concentration results in a strong localization of the excitonic wave function, in an increase in radiative lifetime, and a decrease of the dephasing rate. Local LO-phonon modes caused by the strong modulation of the Cd concentration profile are found in phonon-assisted relaxation processes. Confined biexcitons with large binding energies between 20 and 24 meV are observed, indicating the important role of biexcitons even at room temperature

TRPV4 mediated calcium influx after stretch.

<p>Ca2+ response in NCI-H292 cells 10 s after a single uni-axial cell-stretch to 80% length increase and back to relaxation within 800 ms. Cells were loaded with the Ca²⁺ dye fluo-4 (2<b>μ</b>M) and 0.2% Pluronic F127 (Molecular Probes; Karlsruhe, Germany) and the average fluorescence values of each cell before and 10 s after the strain were determined. The strain-induced change after stimulation was expressed as the % change intensity compared to baseline signal before stretch. (A) Ca²⁺ response 10 s after stretch for 60 seconds. (B) Summary of the mean % Ca²⁺ response from the 60 sec after stretch, a 2.5 fold increase in the [Ca2+]_i was observed that was significantly decreased by 26% with the TRPV4 antagonist (1 <b>μ</b>M) GSK2193874 (184.5 ± 5.07 vs 248.6 ± 10.17). For (A) and (B) data are mean ± SEM; (control n = 121; GSK2193874 n = 94, summary of 13 experiments; ****p ˂ 0.0001 vs control; Unpaired two-tailed t test).</p

TRPV4 mediated stretch-induced cytokine release in macrophages M1 and M2.

<p>Representative experiment of Macrophages seeded on silicoelastic membranes and exposed to cyclic equibiaxial stretch (cyclic 30% strain with 1.25 Hz) for up to 48 h in the presence or absence of the TRPV4-Antagonist GSK2193874 [1<b>μ</b>M]. (A-E) Stretch induced cytokine release in M1 macrophages compared to unstretched control (ctrl) that could be blocked with the TRPV4 antagonist (ant). Stretch induced release of MCP-1 and TNF-α in M2 macrophages that could be blocked by TRPV4 inhibition (F,G). Data are mean ± SEM; (n = 3; *p ˂ 0.05; **p ˂ 0.01; ***p ˂ 0.001; ****p ˂ 0.0001 vs stretch control; one-way ANOVA Tukey's multiple comparisons test).</p

TRPV4 mediated cytokine release.

<p>Representative experiment of NCI-H292 cells incubated for 24 h in the presence or absence of the TRPV4 agonist GSK1016790A [3nM] (ag) with or without pre-treatment with the TRPV4-Antagonist GSK2193874 [1<b>μ</b>M] (ant). (A,B) release of IL-6 and IL-8 through TRPV4 activation compared to medium (ctrl) and DMSO control (veh) that could be blocked by the TRPV4 antagonist. (C,D) TRPV4 mediated release of IL-1α and MDC. Data are mean ± SEM; (n = 6; ****p ˂ 0.0001 vs agonist control; one-way ANOVA Tukey's multiple comparisons test).</p

TRPV4 mediated stretch-induced cytokine release.

<p>Repesentative experiment of NCI-H292 cells seeded on silicoelastic membranes and exposed to cyclic equibiaxial stretch (cyclic 30% strain with 1.25 hz) for 24 h in the presence or absence of the TRPV4-Antagonist GSK2193874 [1<b>μ</b>M]. (A) Stretch induced release of IL-8 compared to unstretched control (ctrl) reduced by 34% with the TRPV4 antagonist (ant) and reduced by 86% with Ruthenium Red (RR). (B) IL-6 release via stretch that was reduced through TRPV4 antagonism by 33% (ant) and reduced by 80% with Ruthenium Red addition (RR). Data are mean ± SEM; (n = 3; *p ˂ 0.05; ****p ˂ 0.0001 vs stretch control; one-way ANOVA Tukey's multiple comparisons test).</p

Concentration-dependent inhibition of TRPV4 effect on Ca²⁺ response.

<p>Representative Ca²⁺-Influx measurement in NCI-H292 cells stimulated with the TRPV4 agonist GSK1016790A (2 nM) and challenged against different concentration of the TRPV4 antagonist GSK2193874 (0.1 nM, 0.3 nM, 1 nM, 3 nM, 10 nM, 30 nM, 100 nM and 300 nM) preincubated for 15 min before agonist addition in the FLIPR^TETRA. Concentration-dependent inhibition of the agonist effect through TRPV4 antagonism with an IC50 of 48,67 nM. Data are mean ± SEM; n = 3.</p