ABSTRACT
The localization dynamics of excitons in organic semiconductors influence the efficiency of charge transfer and separation in these materials. Here we apply time-resolved X-ray absorption spectroscopy to track photoinduced dynamics of a paradigmatic crystalline conjugated polymer: poly(3-hexylthiophene) (P3HT) commonly used in solar cell devices. The πâπ* transition, the first step of solar energy conversion, is pumped with a 15 fs optical pulse and the dynamics are probed by an attosecond soft X-ray pulse at the carbon K-edge. We observe X-ray spectroscopic signatures of the initially hot excitonic state, indicating that it is delocalized over multiple polymer chains. This undergoes a rapid evolution on a sub 50 fs timescale which can be directly associated with cooling and localization to form either a localized exciton or polaron pair.
ABSTRACT
We use a high harmonic generated supercontinuum in the soft X-ray region to measure X-ray absorption near edge structure (XANES) spectra in polythiophene (poly(3-hexylthiophene)) films at multiple absorption edges. A few-cycle carrier-envelope phase-stable laser pulse centered at 1800 nm was used to generate a stable soft X-ray supercontinuum, with amplitude gating limiting the generated pulse duration to a single optical half-cycle. We report a quantitative transmission measurement of the sulfur L2,3 edge over the range 160-200 eV and the carbon K edge from 280 to 330 eV. These spectra show all the features previously reported in the XANES spectra of polythiophene, but for the first time they are measured with a source that has an approximately 1 fs pulse duration. This study opens the door to measurements that can fully time-resolve the photoexcited electronic dynamics in these systems.
ABSTRACT
Since iron can contribute to detrimental radical generating processes through the Fenton and Haber-Weiss reactions, it seems to be a reasonable approach to modulate iron-related pathways in inflammation. In the human organism a counterregulatory reduction in iron availability is observed during inflammatory diseases. Under pathological conditions with reduced or increased baseline iron levels different consequences regarding protection or susceptibility to inflammation have to be considered. Given the role of iron in development of inflammatory diseases, pharmaceutical agents targeting this pathway promise to improve the clinical outcome. The objective of this review is to highlight the mechanisms of iron regulation and iron chelation, and to demonstrate the potential impact of this strategy in the management of several acute and chronic inflammatory diseases, including cancer.
Subject(s)
Inflammation/drug therapy , Iron Chelating Agents/therapeutic use , Animals , Fibrosis , Hemochromatosis/drug therapy , Humans , Inflammation/metabolism , Iron/metabolism , Kidney/pathology , Neoplasms/drug therapy , Reactive Oxygen Species/metabolism , Systemic Inflammatory Response Syndrome/drug therapyABSTRACT
110 infants aged from one to 384 days without cardiovascular diseases were examined by two-dimensional echocardiography. Their body weights were 2.4 to 10 kg. Using mechanical, angular scanheads of 7.5 and 5.0 MHz, the parasternal long and short axes views, the apical long axis view, the suprasternal long and short axes views and the subxiphoidal position was searched. Long axis and short axis of the left ventricle were measured at end-diastole and at end-systole. Aorta, pulmonary artery trunk, left and right pulmonary arteries and the roots of both coronary arteries were measured off-line at end-diastole. To confirm the measurements a) vertical and horizontal diameters of orthogonal transected vessels were measured, b) some vessel diameters were measured in different views and c) 10 infants were examined by two independent observers. The result of this inter-observer examination had an agreement of 77% in the 370 measurements and an inter-observer variability of 2.4%. The measured diameters were linearily related to body weight and BSA in this age group. Also, the calculated areas and volumes of the left ventricle related linearily to body weight and BSA. To simplify the estimation of left ventricular volume a formula was derived id est: Volume of left ventricle = 9.15 x greatest short axis x greatest long axis -20. The following quotients are independent from age, body weight, height, and BSA: Pulmonary artery root/aortic root, pulmonary artery bifurcation/aortic root, pulmonary artery bifurcation/-root, left atrium/aortic root.(ABSTRACT TRUNCATED AT 250 WORDS)
