Intermolecular charge transport in dye monolayers

This thesis reports the experimental investigation of intermolecular charge transport in dye monolayers anchored to the surface of nanocrystalline oxides. I use electrochemistry and transient spectroscopy to measure diffusion of holes within dye monolayers and interpret my observations on the basis of the non-adiabatic Marcus theory of charge transfer. I observe thermally activated hole diffusion for dyes used in dye sensitized solar cells (DSSCs) anchored to TiO2 and immersed in an inert acetonitrile based electrolyte. The corresponding values of reorganization energy of charge transfer between the dyes range between 700 and 1500 meV. Assuming negligible contribution from energetic disorder, this shows agreement with previously reported calculations of reorganization energy. Low outer sphere and low inner sphere reorganization energies correlate with delocalization of the HOMO and with rigid molecular structures showing extended conjugation. I show that hole diffusion in the monolayer can be controlled both at the μm and at the nm scale by varying the fraction of TiO2 surface covered with dyes. I present the effect of decreasing the dye surface coverage and consequently stopping hole diffusion on photo-electrochemical device structures. First, I observe a slowdown of the photo-induced recombination reaction of holes in the dye monolayer to electrons in the TiO2 when decreasing the dye loading. This result is consistent with the hypothesis that hole diffusion in the dye monolayer contributes to faster recombination. Second, I show that hole transport in the dye monolayer is responsible for increased dye regeneration efficiency in solid state DSSCs. I quantify improved regeneration yield by between 50% and 5% depending on the degree of the pore filling by the hole transporting material spiro OMeTAD. Finally I demonstrate that effective photo-conversion can occur in solar cell structures where dye monolayers function as the only hole transport phase.Open Acces

The effects of β1-adrenergic blockade on cardiovascular oxygen flow in normoxic and hypoxic humans at exercise

At exercise steady state, the lower the arterial oxygen saturation (SaO2), the lower the O2 return (\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2}). A linear relationship between these variables was demonstrated. Our conjecture is that this relationship describes a condition of predominant sympathetic activation, from which it is hypothesized that selective β1-adrenergic blockade (BB) would reduce O2 delivery (\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2} ) and \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} . To test this hypothesis, we studied the effects of BB on \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2} and \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} in exercising humans in normoxia and hypoxia. O2 consumption (\ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{2} ), cardiac output (\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}, CO_{2}\; \hbox{rebreathing}), heart rate, SaO2 and haemoglobin concentration were measured on six subjects (age 25.5±2.4years, mass 78.1±9.0kg) in normoxia and hypoxia (inspired O2 fraction of 0.11) at rest and steady-state exercises of 50, 100, and 150W without (C) and with BB with metoprolol. Arterial O2 concentration (CaO2), \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2}, and \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} were then computed. Heart rate, higher in hypoxia than in normoxia, decreased with BB. At each \ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{2} , \ifmmode\expandafter\dot\else\expandafter\.\fi{Q} was higher in hypoxia than in normoxia. With BB, it decreased during intense exercise in normoxia, at rest, and during light exercise in hypoxia. SaO2 and CaO2 were unaffected by BB. The \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2} changes under BB were parallel to those in \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}. \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} was unaffected by exercise in normoxia. In hypoxia the slope of the relationship between \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2} and \ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{2} was lower than 1, indicating a reduction of \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} with increasing workload. \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} was a linear function of SaO2 both in C and in BB. The line for BB was flatter than and below that for C. The resting \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} in normoxia, lower than the corresponding exercise values, lied on the BB line. These results agree with the tested hypothesis. The two observed relationships between \ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} and SaO2 apply to conditions of predominant sympathetic or vagal activation, respectively. Moving from one line to the other implies resetting of the cardiovascular regulatio

The role of hole transport between dyes in solid-state dye-sensitized solar cells

In dye-sensitized solar cells (DSSCs) photogenerated positive charges are normally considered to be carried away from the dyes by a separate phase of hole-transporting material (HTM). We show that there can also be significant transport within the dye monolayer itself before the hole reaches the HTM. We quantify the fraction of dye regeneration in solid-state DSSCs that can be attributed to this process. By using cyclic voltammetry and transient anisotropy spectroscopy, we demonstrate that the rate of interdye hole transport is prevented both on micrometer and nanometer length scales by reducing the dye loading on the TiO₂ surface. The dye regeneration yield is quantified for films with high and low dye loadings (with and without hole percolation in the dye monolayer) infiltrated with varying levels of HTM. Interdye hole transport can account for >50% of the overall dye regeneration with low HTM pore filling. This is reduced to about 5% when the infiltration of the HTM in the pores is optimized in 2 μm thick films. Finally, we use hole transport in the dye monolayer to characterize the spatial distribution of the HTM phase in the pores of the dyed mesoporous TiO₂

Interdye Hole Transport Accelerates Recombination in Dye Sensitized Mesoporous Films

Charge recombination between oxidized dyes attached to mesoporous TiO2 and electrons in the TiO2 was studied in inert electrolytes using transient absorption spectroscopy. Simultaneously, hole transport within the dye monolayers was monitored by transient absorption anisotropy. The rate of recombination decreased when hole transport was inhibited selectively, either by decreasing the dye surface coverage or by changing the electrolyte environment. From Monte Carlo simulations of electron and hole diffusion in a particle, modeled as a cubic structure, we identify the conditions under which hole lifetime depends on the hole diffusion coefficient for the case of normal (disorder free) diffusion. From simulations of transient absorption and transient absorption anisotropy, we find that the rate and the dispersive character of hole transport in the dye monolayer observed spectroscopically can be explained by incomplete coverage and disorder in the monolayer. We show that dispersive transport in the dye monolayer combined with inhomogeneity in the TiO2 surface reactivity can contribute to the observed stretched electron-hole recombination dynamics and electron density dependence of hole lifetimes. Our experimental and computational analysis of lateral processes at interfaces can be applied to investigate and optimize charge transport and recombination in solar energy conversion devices using electrodes functionalized with molecular light absorbers and catalysts

Ionic-to-electronic current amplification in hybrid perovskite solar cells: ionically gated transistor-interface circuit model explains hysteresis and impedance of mixed conducting devices

Mobile ions in hybrid perovskite semiconductors introduce a new degree of freedom to electronic devices suggesting applications beyond photovoltaics. An intuitive device model describing the interplay between ionic and electronic charge transfer is needed to unlock the full potential of the technology. We describe the perovskite-contact interfaces as transistors which couple ionic charge redistribution to energetic barriers controlling electronic injection and recombination. This reveals an amplification factor between the out of phase electronic current and the ionic current. Our findings suggest a strategy to design thin film electronic components with large, tuneable, capacitor-like and inductor-like characteristics. The resulting simple equivalent circuit model, which we verified with time-dependent drift-diffusion simulations of measured impedance spectra, allows a general description and interpretation of perovskite solar cell behaviour

A leukemia-protective germline variant mediates chromatin module formation via transcription factor nucleation

Non-coding variants coordinate transcription factor (TF) binding and chromatin mark enrichment changes over regions spanning >100 kb. These molecularly coordinated regions are named "variable chromatin modules" (VCMs), providing a conceptual framework of how regulatory variation might shape complex traits. To better understand the molecular mechanisms underlying VCM formation, here, we mechanistically dissect a VCM-modulating noncoding variant that is associated with reduced chronic lymphocytic leukemia (CLL) predisposition and disease progression. This common, germline variant constitutes a 5-bp indel that controls the activity of an AXIN2 gene-linked VCM by creating a MEF2 binding site, which, upon binding, activates a super-enhancer-like regulatory element. This triggers a large change in TF binding activity and chromatin state at an enhancer cluster spanning >150 kb, coinciding with subtle, long-range chromatin compaction and robust AXIN2 up-regulation. Our results support a model in which the indel acts as an AXIN2 VCM-activating TF nucleation event, which modulates CLL pathology