D-A(1)-D-A(2) Copolymers with Extended Donor Segments for Efficient Polymer Solar Cells

Typically a donor-acceptor (D-A) design strategy is used for engineering the bandgap of polymers for solar cells. However, in this work, a series of alternating D-A(1-)D-A(2) copolymers PnTQTI(F) were synthesized and characterized with oligothiophenes (nT, n = 1, 2, 3) as the donor and two electron-deficient moieties, quinoxaline and isoindigo, as the acceptors in the repeating unit. We have studied the influence of the donor segments with different numbers of thiophene units and the effect of the addition of fluorine to the quinoxaline unit of the D-A(1)-D-A(2) polymers. The photophysical, electrochemical, and photovoltaic properties of the polymers were examined via a range of techniques and related to theoretical simulations. On increasing the length of the donor thiophene units, broader absorption spectra were observed in addition to a sequential increase in HOMO levels, while the LUMO levels displayed very small variations. The addition of fluorine to the quinoxaline unit not only decreased the HOMO levels of the resulting polymers but also enhanced the absorption coefficients. A superior photovoltaic performance was observed for the P3TQTI-F-based device with a power conversion efficiency (PCE) of 7.0%, which is the highest efficiency for alternating D-A(1)-D-A(2) polymers reported to date. The structureproperty correlations of the PnTQTI(F) polymers demonstrate that varying of the length of the donor segments is a valuable method for designing high-performance D-A(1)-D-A(2) copolymers and highlight the promising nature of D-A(1)-D-A(2) copolymers for efficient bulk-heterojunction solar cells

Time course analysis of mechanical ventilation-induced diaphragm contractile muscle dysfunction in the rat.

Controlled mechanical ventilation (CMV) plays a key role in triggering the impaired diaphragm muscle function and the concomitant delayed weaning from the respirator in critically ill intensive care unit (ICU) patients. To date, experimental and clinical studies have primarily focused on early effects on the diaphragm by CMV, or at specific time points. To improve our understanding of the mechanisms underlying the impaired diaphragm muscle function in response to mechanical ventilation, we have performed time-resolved analyses between 6h and 14days using an experimental rat ICU model allowing detailed studies of the diaphragm in response to long-term CMV. A rapid and early decline in maximum muscle fibre force and preceding muscle fibre atrophy was observed in the diaphragm in response to CMV, resulting in an 85% reduction in residual diaphragm fibre function after 9-14days of CMV. A modest loss of contractile proteins was observed and linked to an early activation of the ubiquitin proteasome pathway, myosin:actin ratios were not affected and the transcriptional regulation of myosin isoforms did not show any dramatic changes during the observation period. Furthermore, small angle X-ray diffraction analyses demonstrate that myosin can bind to actin in an ATP-dependent manner even after 9-14days of exposure to CMV. Thus, quantitative changes in muscle fibre size and contractile proteins are not the dominating factors underlying the dramatic decline in diaphragm muscle function in response to CMV, in contrast to earlier observations in limb muscles. The observed early loss of subsarcolemmal neuronal nitric oxide synthase activity, onset of oxidative stress, intracellular lipid accumulation and post-translational protein modifications strongly argue for significant qualitative changes in contractile proteins causing the severely impaired residual function in diaphragm fibres after long-term mechanical ventilation. For the first time, the present study demonstrates novel changes in the diaphragm structure/function and underlying mechanisms at the gene, protein and cellular levels in response to CMV at a high temporal resolution ranging from 6h to 14days