A generalized model for time-resolved luminescence of localized carriers and applications: Dispersive thermodynamics of localized carriers

Abstract

For excited carriers or electron-hole coupling pairs (excitons) in disordered crystals, they may localize and broadly distribute within energy space first, and then experience radiative recombination and thermal transfer (i.e., non-radiative recombination via multi-phonon process) processes till they eventually return to their ground states. It has been known for a very long time that the time dynamics of these elementary excitations is energy dependent or dispersive. However, theoretical treatments to the problem are notoriously difficult. Here, we develop an analytical generalized model for temperature dependent time-resolved luminescence, which is capable of giving a quantitative description of dispersive carrier dynamics in a wide temperature range. The two effective luminescence and nonradiative recombination lifetimes of localized elementary excitations were mathematically derived as Carrier localization (CL) in real crystalline solids due to various disorders, e.g., defects, impurities, composition fluctuation, lattice distortion etc. is a ubiquitous phenomenon which was theoretically treated by Anderson for the first time 1 . To date, CL and related phenomena still remain as a subject of extensive interest primarily because of their scientific significance and profound impact on electrical, magnetic and optical properties of material systems [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18] . With the rapid development of the InGaN alloy based blue-green light emitting diodes, recently, the CL effect induced by structural imperfections has been increasingly addressed [19][20][21] . For example, it has been well shown that localized carriers due to alloy disorder, especially indium content fluctuation, can produce efficient luminescence and unusual thermodynamic behaviors [19][20][21][22][23][24][25][26][27][28] . In order to interpret these unusual luminescence behaviors associated with the carrier localization, many attempts have been devoted. For example, Eliseev et al. proposed an empirical formula to interpret temperature-induced "blue" shift in peak position of luminescence 25 . This model agrees well with experimental data at high temperatures, but does not work at low temperatures. Wang applied the pseudopotential approach to study the CL mechanism in different InGaN systems 23 , which mainly focuses on the contribution of component fluctuation and quantum-dot formation to the carrier localization.

Airborne PM2.5-Induced Hepatic Insulin Resistance by Nrf2/JNK-Mediated Signaling Pathway

“…In this study, we found that TNF-α levels in serum were increased during the fourth week, but no significant changes were seen during the 12th week (data not shown). These observations are consistent with the previous reports that acute PM exposure significantly increases inflammatory cytokine levels [ 66 ]. There were no significant changes in the levels of inflammatory cytokines after long-term PM 2.5 exposure [ 28 , 67 ].…”

Dual Role of CREB in The Regulation of VSMC Proliferation: Mode of Activation Determines Pro- or Anti-Mitogenic Function

“…Elevation of cAMP with forskolin in various cell types induces CREB phosphorylation at serine-133 and increases CREB-dependent transcription 30 , 44 – 46 . However, these studies use high concentrations of forskolin (typically 10–25 µM), which induce supra-physiological levels of cAMP in VSMC 4 . Consistent with these findings, we were also able to detect increased serine-133 phosphorylation in VSMC stimulated with 25 µM forskolin (Supplement Fig.…”

Markers of acute toxicity of DDT exposure in pancreatic beta-cells determined by a proteomic approach

“…This chaperone interacts with many proteins, including NDUS3 mentioned above [ 33 ]. In mitochondria, GRP75 helps to maintain mitochondrial shape and function [ 34 , 35 ]. The exposure to p , p‘- DDT strongly upregulated expression of GRP75 (see Tables 1 and 2 ), which may suggest that, after the exposure to DDT, mitochondria needed full support to maintain their functionality.…”