Gas dependent hysteresis in MoS2_2 field effect transistors

We study the effect of electric stress, gas pressure and gas type on the hysteresis in the transfer characteristics of monolayer molybdenum disulfide (MoS2) field effect transistors. The presence of defects and point vacancies in the MoS2 crystal structure facilitates the adsorption of oxygen, nitrogen, hydrogen or methane, which strongly affect the transistor electrical characteristics. Although the gas adsorption does not modify the conduction type, we demonstrate a correlation between hysteresis width and adsorption energy onto the MoS2 surface. We show that hysteresis is controllable by pressure and/or gas type. Hysteresis features two well-separated current levels, especially when gases are stably adsorbed on the channel, which can be exploited in memory devices.Comment: 8 pages, 5 figure

Electrodeposited lead dioxide coatings

Lead dioxide coatings on inert substrates such as titanium and carbon now offer new opportunities for a material known for 150 years. It is now recognised that electrodeposition allows the preparation of stable coatings with different phase structures and a wide range of surface morphologies. In addition, substantial modification to the physical properties and catalytic activities of the coatings are possible through doping and the fabrication of nanostructured deposits or composites. In addition to applications as a cheap anode material in electrochemical technology, lead dioxide coatings provide unique possibilities for probing the dependence of catalytic activity on layer composition and structure (critical review, 256 references)

Accelerated apoptotic death and <i>in vivo</i> turnover of erythrocytes in mice lacking functional mitogen- and stress-activated kinase MSK1/2

The mitogen- and stress-activated kinase MSK1/2 plays a decisive role in apoptosis. In analogy to apoptosis of nucleated cells, suicidal erythrocyte death called eryptosis is characterized by cell shrinkage and cell membrane scrambling leading to phosphatidylserine (PS) externalization. Here, we explored whether MSK1/2 participates in the regulation of eryptosis. To this end, erythrocytes were isolated from mice lacking functional MSK1/2 (msk−/−) and corresponding wild-type mice (msk+/+). Blood count, hematocrit, hemoglobin concentration and mean erythrocyte volume were similar in both msk−/− and msk+/+ mice, but reticulocyte count was significantly increased in msk−/− mice. Cell membrane PS exposure was similar in untreated msk−/− and msk+/+ erythrocytes, but was enhanced by pathophysiological cell stressors ex vivo such as hyperosmotic shock or energy depletion to significantly higher levels in msk−/− erythrocytes than in msk+/+ erythrocytes. Cell shrinkage following hyperosmotic shock and energy depletion, as well as hemolysis following decrease of extracellular osmolarity was more pronounced in msk−/− erythrocytes. The in vivo clearance of autologously-infused CFSE-labeled erythrocytes from circulating blood was faster in msk−/− mice. The spleens from msk−/− mice contained a significantly greater number of PS-exposing erythrocytes than spleens from msk+/+ mice. The present observations point to accelerated eryptosis and subsequent clearance of erythrocytes leading to enhanced erythrocyte turnover in MSK1/2-deficient mice

cGMP-Dependent Protein Kinase I Is Crucial for Angiogenesis and Postnatal Vasculogenesis

Background Endothelium-derived nitric oxide plays an important role for the bone marrow microenvironment. Since several important effects of nitric oxide are mediated by cGMP-dependent pathways, we investigated the role of the cGMP downstream effector cGMP-dependent protein kinase I (cGKI) on postnatal neovascularization. Methodology/Principal Findings In a disc neovascularization model, cGKI -/- mice showed an impaired neovascularization as compared to their wild-type (WT) littermates. Infusion of WT, but not cGKI -/- bone marrow progenitors rescued the impaired ingrowth of new vessels in cGKI-deficient mice. Bone marrow progenitors from cGKI -/- mice showed reduced proliferation and survival rates. In addition, we used cGKI alpha leucine zipper mutant (LZM) mice as model for cGKI deficiency. LZM mice harbor a mutation in the cGKI alpha leucine zipper that prevents interaction with downstream signaling molecules. Consistently, LZM mice exhibited reduced numbers of vasculogenic progenitors and impaired neovascularization following hindlimb ischemia compared to WT mice. Conclusions/Significance Our findings demonstrate that the cGMP-cGKI pathway is critical for postnatal neovascularization and establish a new role for cGKI in vasculogenesis, which is mediated by bone marrow-derived progenitors

Oberflächenphotospannung und Kontaktpotentialdifferenz von hydrogeniertem amorphen Silizium

The contact potential difference (CPD) and the surface photovoltage (SPV) were measured by the Kelvin technique on hydrogenated amorphous silicon (a-Si:H) films. A vacuum lock allowed the transfer of a-Si :N films from the glow discharge system to the analysis chamber without surface contamination. For highly phosphorous-doped films, the comparison of the temperature dependence of the electrical conductivity a and the CPD demonstrates that the temperature dependence of both quantities is dominated by the position of the Fermi level EF in the bulk. E$_{vac}$-E$_{F}$ determined by CPD shows kinks at the same temperatures as E$_{c}$-E$_{F}$ obtained from the conductivity (E$_{vac}$ : vacuum level, E$_{C}$ : mobility edge). The present results confirm the previous conjecture stating that the variation of E$_{c}$-E$_{F}$ is due to a non-linear statistical Fermi level shift. No correlation is observed between a and CPD for undoped films suggesting that in this case the temperature dependence of CPD is mainly determined by occupation statistics of surface or surface-near states. The surface photovoltage measurements indicate a surface depletion layer for undoped films and flat-band conditions for highly doped films. For a given temperature (T = 230 - 270 K) and photon energy the SPV shows always a logarithmic dependence on light intensity at low intensity values and a saturation at high intensity. Analysis of the results for homogeneous illumination of the sample (E$_{ph}$ = 2 eV) shows that the SPV here is due to a change of band bending via interaction of bulk-generated carriers with surface states. The saturation value of the SPV reflects the band bending in the dark. For illumination by 2.5 eV, on the other hand, (i. e. when the light is absorbed in a thin surface layer) a considerably higher saturation value than for E$_{ph}$ = 2 eV is observed. This increase is attributed to the Dember effect

Inhibitory effect of thymol on suicidal erythrocyte death

The antibacterial plant component thymol has antioxidant activity. Oxidative stress is known to activate Ca 2+ -permeable cation channels with subsequent Ca 2+ entry, activation of Ca 2+ -sensitive K + channels, cell shrinkage, cell membrane scrambling and phosphatidylserine exposure at the erythrocyte surface. Cell shrinkage and phosphatidylserine exposure are typical features of suicidal erythrocyte death or eryptosis. Eryptotic cells are cleared from circulating blood thus causing anemia and may adhere to the vascular wall thus interfering with the microcirculation. The present experiments explored whether thymol interacts with eryptosis. Annexin V-binding was utilized to determine phosphatidylserine exposure, forward scatter to detect alterations of cell volume and Fluo3 fluorescence to depict changes of the cytosolic Ca 2+ activity. Oxidative stress (30 min. 0.3 mM tert-butylhydroperoxide), energy depletion (48 h glucose removal) and isotonic cell shrinkage (48 h replacement of extracellular Cl - with gluconate) significantly increased annexin V-binding and decreased the forward scatter, effects significantly blunted in the presence of thymol 2.5-20 μg/ml. Thymol is a potent inhibitor of suicidal erythrocyte death particularly following oxidative stress. In conclusion, thymol may be useful incounteracting anemia and impairment of microcirculation. Copyright © 2009 S. Karger AG, Basel

MEASUREMENTS OF ARRIVAL TIME DISTRIBUTIONS OF EAS MUONS WITH THE FACILITIES OF THE KASCADE CENTRAL DETECTOR

The central detector of the KASCADE experiment is equipped with a trigger and timing facility, which enables measurements of the arrival time distributions of muons hitting the central detector. The muons are identified with an energy threshold of 2 GeV by a setup of multiwire proportional chambers, positioned below the hadron calorimeter. The features of the muon arrival time distributions have been studied with EAS simulations. Advanced methods for the analysis of arrival times of EAS particles, based on Bayes decision rules and statistical techniques analysing nonparametric multivariate distributions, have been developed. First experimental results of the arrival time distributions of the first EAS muon, the median and mean values and the dispersion, their dependencies on and correlations with various shower variables are presented