Electron-hole pairs during the adsorption dynamics of O2 on Pd(100) - Exciting or not?

During the exothermic adsorption of molecules at solid surfaces dissipation of the released energy occurs via the excitation of electronic and phononic degrees of freedom. For metallic substrates the role of the nonadiabatic electronic excitation channel has been controversially discussed, as the absence of a band gap could favour an easy coupling to a manifold of electronhole pairs of arbitrarily low energies. We analyse this situation for the highly exothermic showcase system of molecular oxygen dissociating at Pd(100), using time-dependent perturbation theory applied to first-principles electronic-structure calculations. For a range of different trajectories of impinging O2 molecules we compute largely varying electron-hole pair spectra, which underlines the necessity to consider the high-dimensionality of the surface dynamical process when assessing the total energy loss into this dissipation channel. Despite the high Pd density of states at the Fermi level, the concomitant non-adiabatic energy losses nevertheless never exceed about 5% of the available chemisorption energy. While this supports an electronically adiabatic description of the predominant heat dissipation into the phononic system, we critically discuss the non-adiabatic excitations in the context of the O2 spin transition during the dissociation process.Comment: 20 pages including 7 figures; related publications can be found at http://www.fhi-berlin.mpg.de/th/th.html [added two references, changed V_{fsa} to V_{6D}, modified a few formulations in interpretation of spin asymmetry of eh-spectra, added missing equals sign in Eg.(2.10)

Residual platelet ADP reactivity after clopidogrel treatment is dependent on activation of both the unblocked P2Y1 and the P2Y12 receptor and is correlated with protein expression of P2Y12

Two ADP receptors have been identified on human platelets: P2Y1 and P2Y12. The P2Y12 receptor blocker clopidogrel is widely used to reduce the risks in acute coronary syndromes, but, currently, there is no P2Y1 blocker in clinical use. Evidence for variable responses to clopidogrel has been described in several reports. The mechanistic explanation for this phenomenon is not fully understood. The aim of this study was to examine mechanisms responsible for variability of 2MeS-ADP, a stable ADP analogue, induced platelet reactivity in clopidogrel-treated patients. Platelet reactivity was assessed by flow cytometry measurements of P-selectin (CD62P) and activated GpIIb/IIIa complex (PAC-1). Residual 2MeS-ADP activation via the P2Y12 and P2Y1 receptors was determined by co-incubation with the selective antagonists AR-C69931 and MRS2179 in vitro. P2Y1 and P2Y12 receptor expression on both RNA and protein level were determined, as well as the P2Y12 H1 or H2 haplotypes. Our data suggest that the residual platelet activation of 2MeS-ADP after clopidogrel treatment is partly due to an inadequate antagonistic effect of clopidogrel on the P2Y12 receptor and partly due to activation of the P2Y1 receptor, which is unaffected by clopidogrel. Moreover, a correlation between increased P2Y12 protein expression on platelets and decreased response to clopidogrel was noticed, r2=0.43 (P<0.05). No correlation was found between P2Y12 mRNA levels and clopidogrel resistance, indicating post-transcriptional mechanisms. To achieve additional ADP inhibition in platelets, antagonists directed at the P2Y1 receptor could be more promising than the development of more potent P2Y12 receptor antagonists

Protection of flunarizine on cerebral mitochondria injury induced by cortical spreading depression under hypoxic conditions

A rat cortical spreading depression (CSD) model was established to explore whether cerebral mitochondria injury was induced by CSD under both normoxic and hypoxic conditions and whether flunarizine had a protective effect on cerebral mitochondria. SD rats, which were divided into seven groups, received treatment as follows: no intervention (control Group I); 1 M NaCl injections (Group II); 1 M KCl injections (Group III); intraperitoneal flunarizine (3 mg/kg) 30 min before KCl injections (Group IV); 14% O2 inhalation before NaCl injections (Group V); 14% O2 inhalation followed by KCl injections (Group VI); 14% O2 inhalation and intraperitoneal flunarizine followed by KCl injections (Group VII). Following treatment, brains were removed for the analysis of mitochondria transmembrane potential (MMP) and oxidative respiratory function after recording the number, amplitude and duration of CSD. The duration of CSD was significantly longer in Group VI than that in Group III. The number and duration of CSD in Group VII was significantly lower than that in Group VI. MMP in Group VI was significantly lower than that in Group III, and MMP in Group VII was significantly higher than that in Group VI. State 4 respiration in Group VI was significantly higher than that in Group III, and state 3 respiration in Group VII was significantly higher than that in Group VI. Respiration control of rate in Group VII was also significantly higher than that in Group VI. Thus, we concluded that aggravated cerebral mitochondria injury might be attributed to CSD under hypoxic conditions. Flunarizine can alleviate such cerebral mitochondria injury under both normoxic and hypoxic conditions

Surgical Treatment for Agenesis of the Vena Cava: A Single-centre Experience in 15 Cases

AbstractObjectiveAgenesis of the inferior vena cava (IVC) is a rare vascular malformation. Deep vein thrombosis (DVT) and bilateral pelvic thrombosis develop quite frequently, making surgical therapy necessary.Patients and methodsBetween 1982 and 2006, 15 patients (nine male, six female, mean age 28 standard deviance 9 years) with agenesis of the IVC (IVCA) were treated surgically because of acute or subacute DVT. These patients underwent bilateral transfemoral ante- and retrograde thrombectomy of the iliofemoral and sometimes popliteal veins and replacement of the IVC with an external ring supported PTFE-graft. Bi- or unilateral arteriovenous fistulae were created in the femoral region. The fistulae were closed, on average, 8 months after trans-arterial venography was performed. These patients were examined clinically and by duplex ultrasound imaging during follow-up to assess graft patency and to allow CEAP classification. Patients were assessed for the development of post-thrombotic syndrome (PTS).ResultsNo patient died during any part of their treatment or within 60 days. Primary patency of the venous reconstruction was 53%, secondary and long time follow-up patency was 83%. The mean duration of follow-up was 41 SD 12 months. Minor complications were observed in five cases (33%). PTS showed no progression during a follow-up of 41 SD 12 months in all patients. There was no change in the CEAP clinical stage during follow-up nor did any leg ulcer develop.ConclusionA surgical approach to restore venous patency is effective and appears to prevent the deterioration of CVI over time