Coexisting large and small vessel disease in patients with ischemic stroke of undetermined cause

Background and Purpose: Large artery atherosclerosis (LAA) and small vessel disease (SVD) share common risk factors for stroke. We aimed at investigating the association of SVD with cerebral LAA as well as with atherosclerosis in patients with stroke likely to originate from aortic plaques. Methods: We investigated 71 consecutive patients (48 men, mean age 64.2 +/- 13 years) with ischemic stroke of undetermined cause according to the ASCO classification, who received ECG-triggered CT angiography for best available atherosclerotic plaque detection in the aorta. Results: Aortic atherosclerotic plaques were detected in 54 patients (76.1%). The presence of SVD significantly correlated with the presence of aortic plaques (p < 0.001), as well as LAA (p < 0.001) and risk factors such as arterial hypertension (p = 0.032) and diabetes mellitus (p = 0.017). Conclusions: Aortic plaques are common in patients with stroke of undetermined cause. If so, SVD and LAA are often coexisting, which demonstrates the close link of macro- and microangiopathy, at least in cases of severe risk factors of atherosclerosis. Copyright © 2012 S. Karger AG, Base

Optical Control of Field-Emission Sites by Femtosecond Laser Pulses

We have investigated field emission patterns from a clean tungsten tip apex induced by femtosecond laser pulses. Strongly asymmetric modulations of the field emission intensity distributions are observed depending on the polarization of the light and the laser incidence direction relative to the azimuthal orientation of tip apex. In effect, we have realized an ultrafast pulsed field-emission source with site selectivity on the 10 nm scale. Simulations of local fields on the tip apex and of electron emission patterns based on photo-excited nonequilibrium electron distributions explain our observations quantitatively.Comment: 4 pages, submitted to Physical Review Letter

A centrality measure for quantifying spread on weighted, directed networks

While many centrality measures for complex networks have been proposed, relatively few have been developed specifically for weighted, directed (WD) networks. Here we propose a centrality measure for spread (of information, pathogens, etc.) through WD networks based on the independent cascade model (ICM). While deriving exact results for the ICM requires Monte Carlo simulations, we show that our centrality measure (Viral Centrality) provides excellent approximation to ICM results for networks in which the weighted strength of cycles is not too large. We show this can be quantified with the leading eigenvalue of the weighted adjacency matrix, and we show that Viral Centrality outperforms other common centrality measures in both simulated and empirical WD networks.Comment: 3 figure

CT angiography of the aorta is superior to transesophageal echocardiography for determining stroke subtypes in patients with cryptogenic ischemic stroke

Background: The etiology of ischemic strokes remains cryptogenic in about one third of patients, even after extensive workup in specialized centers. Atherosclerotic plaques in the aorta can cause thromboembolic events but are often overlooked. They can elude standard identification by transesophageal echocardiography (TEE), which is invasive or at best uncomfortable for many patients. CT angiography (CTA) can be used as an alternative or in addition to TEE if this technique fails to visualize every part of the aorta and in particular the aortic arch. Methods: We prospectively studied 64 patients (47 men, age 60 8 13 years) classified as having cryptogenic stroke after standard and full workup [including brain MRI and 24-hour electrocardiogram (ECG)] with ECG-triggered CTA of the aorta in search of plaques and compared the results with those of TEE. Investigators were blinded to the results of both techniques

Mg3(Bi,Sb)2 single crystals towards high thermoelectric performance

The rapid growth of the thermoelectric cooler market makes the development of novel room temperature thermoelectric materials of great importance. Ternary n-type Mg3(Bi,Sb)2 alloys are promising alternatives to the state-of-the-art Bi2(Te,Se)3 alloys but grain boundary resistance is the most important limitation. n-type Mg3(Bi,Sb)2 single crystals with negligible grain boundaries are expected to have particularly high zT but have rarely been realized due to the demanding Mg-rich growth conditions required. Here, we report, for the first time, the thermoelectric properties of n-type Mg3(Bi,Sb)2 alloyed single crystals grown by a one-step Mg-flux method using sealed tantalum tubes. High weighted mobility ∼140 cm2 V−1 s−1 and a high zT of 0.82 at 315 K are achieved in Y-doped Mg3Bi1.25Sb0.75 single crystals. Through both experimental angle-resolved photoemission spectroscopy and theoretical calculations, we denote the origin of the high thermoelectric performance from a point of view of band widening effect and electronegativity, as well as the necessity to form high Bi/Sb ratio ternary Mg3(Bi,Sb)2 alloys. The present work paves the way for further development of Mg3(Bi,Sb)2 for near room temperature thermoelectric applications

Solution Equilibrium Studies of Anticancer Ruthenium(II)-η6-p-cymene Complexes of Pyridinecarboxylic Acids

Stoichiometry and stability of antitumor ruthenium(II)-η6-p-cymene complexes of picolinic acid and its 6-methyl and 6-carboxylic acid derivatives were determined by pH-potentiometry, 1H NMR spectroscopy and UV–Vis spectrophotometry in aqueous solution in the presence or absence of coordinating chloride ions. The picolinates form exclusively mono-ligand complexes in which they can coordinate via the bidentate (O,N) mode and a chloride or a water molecule is found at the third binding site of the ruthenium(II)-η6-p-cymene moiety depending on the conditions. [Ru(η6-p-cymene)(L)(H2O/Cl)] species are predominant at physiological pH in all studied cases. Hydrolysis of the aqua complex or the chlorido/hydroxido co-ligand exchange results in the formation of the mixed-hydroxido species [Ru(η6-p-cymene)(L)(OH)] in the basic pH range. There is no indication for the decomposition of the mono-ligand complexes during 24 h in the ruthenium(II)-η6-p-cymene-picolinic acid system between pH 3 and 11; however, a slight dissociation with a low reaction rate was found in the other two systems leading to the appearance of the dinuclear trihydroxido-bridged species [Ru2(η6-p-cymene)2(OH)3]+ and free ligands at pH > 10. The replacement of the chlorido by an aqua ligand in [Ru(η6-p-cymene)(L)Cl] was also monitored and equilibrium constants for the exchange process were determined

Induction of JNK and c-Abl signalling by cisplatin and oxaliplatin in mismatch repair-proficient and -deficient cells

Loss of DNA mismatch repair has been observed in a variety of human cancers. Recent studies have shown that loss of DNA mismatch repair results in resistance to cisplatin but not oxaliplatin, suggesting that the mismatch repair proteins serve as a detector for cisplatin but not oxaliplatin adducts. To identify the signal transduction pathways with which the detector communicates, we investigated the effect of loss of DNA mismatch repair on activation of known damage-responsive pathways, and recently reported that cisplatin differentially activates c-Jun NH2-terminal kinase (JNK) and c-Abl in repair-proficient vs.-deficient cells. In the current study, we directly compared differential activation of these pathways by cisplatin vs. oxaliplatin. The results confirm that cisplatin activates JNK kinase 5.7 ± 1.5 (s.d.)-fold more efficiently in DNA mismatch repair-proficient than repair-deficient cells, and that the c-Abl response to cisplatin is completely absent in DNA mismatch repair-deficient cells. In contrast, there was no detectable activation of the JNK or c-Abl kinases in DNA mismatch repair-proficient or -deficient cells exposed to oxaliplatin. The present study demonstrates that, despite the similarity of the adducts produced by cisplatin and oxaliplatin, they appear to be recognized by different detectors. The DNA mismatch repair system plays an important part in the recognition of cisplatin adducts, and activation of both the JNK and c-Abl kinases in response to cisplatin damage is dependent on the detector function of the DNA mismatch repair proteins. In contrast, this detector does not respond to oxaliplatin adducts. © 1999 Cancer Research Campaig