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Notes: Near solid density plasmas have been obtained by the interaction of ultraintense (2×1018 W cm−2) clean laser pulses with targets composed of different thickness of Al on a Si substrate. The depth of the x-ray emission and spectral shapes were measured using x-ray spectroscopy, which simultaneously characterized the emitting plasma and the suprathermal electron distribution. Strong modifications of the plasmas thermal radiative properties have been observed, for the first time, by changing the laser polarization from S to P. This correlates with an increase of suprathermal electrons production. © 2001 American Institute of Physics.

Notes: We present results of the characterization of an ultrafast x-ray streak camera, based on Photonis (formerly Philips Photonics) P860 tube, developed for use in ultrashort laser-produced plasma research. The streak camera presented here (called PX1) has been extensively characterized with continuous and pulsed x-ray sources. Time resolution of 350 fs in the keV x-ray range has been achieved, while maintaining a high spatial resolution of 40 μm along a direction perpendicular to the time dispersion axis. It is shown that the streak camera response is lower when the photocathode is illuminated by a pulsed source than when used with a continuous one. This effect seems to be related to a change in the phosphor response. The camera has been used to achieve high-resolution subpicosecond time-resolved spectroscopy of ultrashort laser plasmas allowing the measurements of K-shell line emission durations of 700 fs. © 2000 American Institute of Physics.

Notes: Abstract: Pharmacologic activation of endogenous protein kinase C (PKC) together with elevation of the intracellular Ca2+ level was previously shown to cause reduction of two voltage-dependent K+ currents (IA and Ica2+-K+) across the soma membrane of the type B photoreceptor within the eye of the mollusc Hermissenda crassicornis. Similar effects were also found to persist for days after acquisition of a classically conditioned response. Also, the state of phosphorylation of a low-molecular-weight protein was changed only within the eyes of conditioned Hermissenda. To examine the role of PKC in causing K+ current changes as well as changes of phosphorylation during conditioning (and possibly other physiologic contexts), we studied here the effects of endogenous PKC activation and exogenous PKC injection on phosphorylation and K+ channel function. Several phosphoproteins (20, 25, 56, and 165 kilodaltons) showed differences in phosphorylation in response to PKC activators applied to intact nervous systems or to isolated eyes. Specific differences were observed for membrane and cytosolic fractions in response to both the phorbol ester 12-deoxyphorbol 13-isobutyrate 20-acetate (DPBA) or exogenous PKC in the presence of Ca2+ and phosphatidylserine/diacylglycerol. Type B cells pretreated with DPBA responded to PKC injection with a persistent reduction of K+ currents. In the absence of DPBA, PKC injection also caused K+ current reduction only following Ca2+ loading conditions. However, the direct effect of PKC injection in the absence of DPBA was only to increase ICa2+_K+. According to a proposed model, the amplitude of the K+ currents would depend on the steady-state balance of effects mediated by PKC within the cytoplasm and membrane-associated PKC. The model further specifies that the effects on K+ currents of cytoplasmic PKC require an intervening proteolytic step. Such a model predicts that increasing the concentration of cytoplasmic protease, e.g., with trypsin, will increase K+ currents, whereas blocking endogenous protease, e.g., with leupeptin, will decrease K+ currents. These effects should be opposed by preexposure of the cells to DPBA. Furthermore, prior injection of leupeptin should block or reverse the effects of subsequent injection of PKC into the type B cell. All of these predictions were confirmed by results reported here. Taken together, the results of this and previous studies suggest that PKC regulation of membrane excitability critically depends on its cellular locus. The implications of such function for long-term physiologic transformations are discussed.

Notes: Summary The squid giant axon responded to a transection injury by producing a gradient of cytoplasmic and vesicular changes at the cut end. At the immediate opening of the cut axon the cytoplasm was fragmented and dispersed and the vesicles in this region were in rapid Brownian movement. Approximately 0.1 mm further in, at the site of maximal axonal constriction, the axoplasm was condensed into a compact, constricted mass containing many large vesicles. The axoplasm was normal a few millimetres beyond this constricted, vesiculated end. It appears that transection triggered the transformation of normal axoplasm into a tightly constricted, highly vesiculated structure. This modified axoplasm at the cut end may slow the spread of damage and degeneration by preventing the bulk outflow of axoplasm, by slowing down the loss of intracellular molecules and by slowing down the influx of destructive extracellular ions (like calcium and chloride).