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The mechanism of photoluminescence (PL) quenching of thin amorphous N,N'-bis(3-methylphenyl)- N,N'-bis(phenyl)benzidine (TPD) films exposed to UV light in air is studied. TPD is small organic molecule widely used in production of organic light emmiting devices (OLEDs). Photoluminescence of TPD films decays exponentially with time of irradiation, i.e. with the increase of concentration of impurities (photo-oxidized TPD molecules) generated by UV irradiation in air. Intensity of PL decreases to half of its original value when the concentration of impurities reaches 0.4%. Average distance between impurities (acceptors) is almost an order of magnitude larger than average distance between host TPD molecules (donors). Direct long range Forster energy transfer is ruled out as the mechanism of PL quenching, as the overlap between donor and acceptor is lacking, and exciton self-diffusion in TPD films is postulated for the mechanism. The presence of oxidation products is confirmed by infrared (IR) spectroscopy. Vibrational spectra of TPD molecule and few other possible products of photo-oxidation of TPD molecule, obtained by density functional theory, are compared to experimental IR spectra.

Background/Aim. Transcranial magnetic stimulation (TMS) is a standard technique for noninvasive assessment of changes in central nervous system excitability. The aim of this study was to examine changes in responses to TMS in patients suffering from Parkinson’s disease (PD) during sustained submaximal isometric voluntary contraction [60% of maximal voluntary contraction (MVC)] of the adductor pollicis muscle, as well as during a subsequent recovery period. Methods. Cortical excitability was tested by single TMS pulses of twice of the motor threshold intensity applied over the vertex. Testing was carried out during the sustained contraction phase every 10 s before and every 5 s after the endurance point, as well as at rest and during brief 60% MVC contractions before (control), immediately after the sustained contraction, and at 5 min intervals during the recovery period. Results. Although the PD patients could sustain the contraction at the required level for as long period of time as the healthy subjects (though contraction level subsided more rapidly after the endurance point), effects of muscle fatigue on the responses to TMS were different. In contrast to the findings observed in the healthy people where motor evoked potentials (MEP) and EMG silent period (SP) in fatigued muscle gradually diminished during contraction up to the endurance point, and increased thereafter, in the majority of patients no changes occurred in MEP size (peak and area) of the adductor pollicis muscle, either before or after the endurance point. On the other hand, changes in the SP of this muscle differed among the subjects, showing a gradual increase, a decrease or no changes in duration. The trends of changes in both MEP size and SP duration in the musculus brachioradialis varied among the tested PD patients, without any consistent pattern, which was in contrast with the findings in the healthy people where both measures showed a gradual increase from the beginning of the sustained contraction. A complete dissociation between changes in MEP and SP during fatigue was also of note, which differed sharply from the findings in the healthy people in who fatigue induced changes in these measures followed identical patterns. Conclusion. These results in the PD patients suggest the presence of impairment and/or compensatory changes in mechanisms responsible for adaptation of voluntary drive as well as for matching between cortical excitation and inhibition which become manifest in demanding motor tasks such as those imposed by muscle fatigue.