Titanium dioxide (TiO 2 ) semiconductors are widely used in energy conversion, energy storage, catalysis, and other electronic applications. Hydrothermally grown TiO 2 nanowires are an alternative to mesoporous TiO 2 nanostructures due to possible direct charge transport, but their full potential waits to be unleashed. Latest findings show a peculiar defect structure, consisting of small single‐crystalline fingers and free internal surfaces, which supposedly promote a number of loss mechanisms. In this paper, the influence of these defects on charge transport is studied on the basis of hybrid solar cells featuring a TiO 2 /dye/polymer interface. Electrical, optical, and structural characterization identifies a number of loss mechanisms, which are inhibited by the introduction of particular annealing steps at specific processing points during fabrication. An increase in power‐conversion efficiency of 35% is obtained, resulting in 2.71% and surpassing mesoporous films of the same material combination. These results suggest that caution has to be exercised when dealing with defect structures possibly present in metal oxides which appear single‐crystalline by conventional analysis methods.

AIMS:Increased myocardial wall strain triggers the cardiac hypertrophic response by increasing cardiomyocyte size, reprogramming gene expression, and enhancing contractile protein synthesis. The LIM protein, migfilin, is a cytoskeleton-associated protein that was found to translocate in vitro into the nucleus in a Ca(2+)-dependent manner, where it co-activates the pivotal cardiac transcription factor Csx/Nkx2.5. However, the in vivo role of migfilin in cardiac function and stress response is unclear.METHODS AND RESULTS:To define the role of migfilin in cardiac hypertrophy, we induced hypertension by transverse aortic constriction (TAC) and compared cardiac morphology and function of migfilin knockout (KO) with wild-type (WT) hearts. Heart size and myocardial contractility were comparable in untreated migfilin KO and WT hearts, but migfilin-null hearts presented a reduced extent of hypertrophic remodelling in response to chronic hypertensile stress. Migfilin KO mice maintained their cardiac function for a longer time period compared with WT mice, which presented extensive fibrosis and death due to heart failure. Migfilin translocated into the nucleus of TAC-treated cardiomyocytes, and migfilin KO hearts showed reduced Akt activation during the early response to pressure overload.CONCLUSIONS:Our findings indicate an important role of migfilin in the regulation of cardiac hypertrophy upon experimental TAC.

Background: Pulse wave velocity is a measure of aortic stiffness and an independent predictor of cardiovascular morbidity and mortality. Adiponectin is involved in atherosclerosis and inflammation. In the present study we aimed to explore the association between plasma adiponectin concentrations and pulse wave velocity in the acute phase after ST-segment elevation myocardial infarction (STEMI).Methods: Forty-six consecutive STEMI patients (mean age 57 +/- 11 years) treated with primary percutaneous coronary intervention (PCI) were enrolled in this cross-sectional study. Plasma adiponectin was measured 2 days after index event by enzyme-linked immunosorbent assay. Aortic pulse wave velocity (PWV) was calculated by the transit-time method with the use of a velocity-encoded, phase-contrast cardiac magnetic resonance protocol.Results: Median plasma adiponectin concentration was 2385 ng/ml (interquartile range 1735-5403). Males had lower plasma adiponectin values than females and current smokers had lower values than non-smokers (all p < 0.02). Adiponectin was significantly associated with PWV (r=0.505, p < 0.001), age (r=0.437, p=0.002), and total cholesterol (r=0.468, p=0.001). Multiple linear regression analysis revealed adiponectin as a predictor of PWV independently of age, sex, smoking status, total cholesterol, and N-terminal pro-B-type natriuretic peptide (p=0.027).Conclusions: Plasma adiponectin concentrations are strongly associated with aortic stiffness in patients after acute STEMI treated with primary PCI. Our data support a possible role for adiponectin as an independent risk marker for increased aortic stiffness in STEMI patients.