Tuning the performance of organic spintronic devices using x-ray generated traps.

X rays produced during electron-beam deposition of metallic electrodes drastically change the performance of organic spintronic devices. The x rays generate traps with an activation energy of ≈0.5 eV in a commonly used organic. These traps lead to a dramatic decrease in spin-diffusion length in organic spin valves. In organic magnetoresistive (OMAR) devices, however, the traps strongly enhance magnetoresistance. OMAR is an intrinsic magnetotransport phenomenon and does not rely on spin injection. We discuss our observations in the framework of currently existing theories.

[The frequency of resuming work among patients with ischemic heart disease after the second phase of rehabilitation]. / Czestosc powrotów do pracy zawodowej chorych na chorobe niedokrwienna serca po drugim etapie rehabilitacji.

The aim of the study was to evaluate the frequency of resuming work among IHD patients after stationary posthospital rehabilitation. 30 patients after MI and revascularisation operations were taken into consideration: A-13 patients who resumed work and B-17 who did not do so. 30 healthy, working men (KZ) were used as a control. ECHO and exercise tests were carried out before and after rehabilitation. The following parameters were analysed: EF%, and HR, SBP, DBP and Dp both rest and exercise, Lt (wat), VO2 and MET, EF% was found to be lower in A and B groups compared to KZ. In both study groups physical efficiency before treatment was low, but after rehabilitation there was a significant increase in efficiency parameters. Consequently, the A group were classified in medium levels, whereas group B remained in low efficiency class. VO2, MET and Lt after rehabilitation in A group were significantly higher compared to those in the B group. 43% of all patients tested resumed work. People with higher education prevailed in the group who resumed work.

Prostaglandin H2 directly lowers human platelet cAMP levels.

In the present study we investigated the ability of prostaglandin H2 (PGH2) to lower platelet cAMP levels independent of thromboxane A2 (TXA2) production. Human platelet-rich plasma was incubated (37 degrees C) with 13 nM prostacyclin (PGI2) to increase platelet cAMP levels. Addition of 500 microM arachidonic acid (AA) to PGI2-treated platelets resulted in a return of cAMP to control levels. Inhibition of both PGH2 and TXA2 production with indomethacin (20 microM) blocked the ability of AA to lower PGI2-stimulated increases in cAMP. On the other hand, selective inhibition of TXA2 production with the thromboxane synthetase blocker 7-(1 imidazoyl) heptanoic acid (7-IHA; 10 microM), did not prevent the cAMP lowering effect of added AA. These results provide evidence that PGH2 need not be converted to TXA2 in order to reduce platelet cAMP levels.

The thromboxane antagonist, 13-azaprostanoic acid, inhibits arachidonic acid-induced Ca2+ release from isolated platelet membrane vesicles.

In the present study we investigated the ability of the arachidonic acid metabolites, prostaglandin H2 and thromboxane A2, to release Ca2+ from isolated platelet vesicles. The vesicles were prepared through modification of previously described procedures. 45Ca uptake and release were determined by Millipore filtration and isotope counting of the filter paper. Incubation of the vesicles (25 degrees C) with 50 microM CaCl2 (plus 45Ca) resulted in the accumulation of 13 nmol Ca2+ per mg of protein under steady-state conditions. Addition of arachidonic acid (25 microM) resulted in a 42% release of the accumulated Ca2+ and the production of 150 ng thromboxane B2/mg protein. Pretreatment of the vesicles with indomethacin (4 microM) completely inhibited arachidonic acid-induced Ca2+ release and reduced thromboxane B2 synthesis by 82%. Pretreatment of the vesicles with the specific thromboxane A2/prostaglandin H2 antagonist, 13-azaprostanoic acid (20 microM), also resulted in complete inhibition of Ca2+ release but no inhibition of thromboxane B2 production. Addition of prostaglandin H2 (0.3 microM) to the platelet vesicles produced a significant release of Ca2+ only in the presence of the adenylate cyclase inhibitor, 2',5'-dideoxyadenosine (100 microM). This Ca2+ release was totally blocked by 13-azaprostanoic acid (20 microM). The thromboxane synthetase inhibitor 9,11-azoprosta-5,13-dienoic acid (azo analog I, 3.6 microM), in the presence of 2',5'-dideoxyadenosine, only slightly inhibited Ca2+ release in response to added prostaglandin H2, even though thromboxane B2 production was blocked by 95%.