Atomic physics modeling of transmission spectra of Sc-doped aerogel foams to support OMEGA experiments.

We present synthetic transmission spectra generated with PrismSPECT utilizing both the ATBASE model and the Los Alamos opacity library (OPLIB) to evaluate whether an alternative choice in atomic data will impact modeling of experimental data from radiation transport experiments using Sc-doped aerogel foams (ScSi6O12 at 75 mg/cm3 density). We have determined that in the 50-200 eV Te range there is a significant difference in the 1s-3p spectra, especially below 100 eV, and for Te = 200 eV above 5000 eV in photon energy. Examining synthetic spectra generated using OPLIB with 300 resolving power reveals spectral sensitivity to Te changes of ∼3 eV.

Measurements of electron transport in foils irradiated with a picosecond time scale laser pulse.

The heating of solid foils by a picosecond time scale laser pulse has been studied by using x-ray emission spectroscopy. The target material was plastic foil with a buried layer of a spectroscopic tracer material. The laser pulse length was either 0.5 or 2 ps, which resulted in a laser irradiance that varied over the range 10(16)-10(19) W/cm(2). Time-resolved measurements of the buried layer emission spectra using an ultrafast x-ray streak camera were used to infer the density and temperature conditions as a function of laser parameters and depth of the buried layer. Comparison of the data to different models of electron transport showed that they are consistent with a model of electron transport that predicts the bulk of the target heating is due to return currents.

Membrane damage and the Ca(2+)-paradox in the perfused rat kidney.

Lactate dehydrogenase (LDH) leaks from the perfused rat kidney under the artificial conditions of a Ca(2+)-paradox protocol, namely Ca(2+)-repletion following a 20 minute period of Ca(2+)-depletion. LDH leakage was markedly suppressed by perfusion at 25 degrees C or with 0.1 mM dibucaine or 2 mM lidocaine. Lidocaine inhibited leakage only during Ca(2+)-depletion. Lowering the perfusion rate significantly reduced LDH escape. No LDH loss occurred if the osmotic pressure of the perfusion fluid was raised by 420 mOsm during either Ca(2+)-depletion or Ca(2+)-repletion. Amiloride (2 mM) significantly reduced LDH leakage to 43%. Reduction of the pH of the perfusion fluid to 6.8 significantly inhibited LDH loss, and at pH 6.4 this leakage was almost completely suppressed. LDH loss was equally suppressed at pH 6.4 only during Ca(2+)-depletion, whereas pH 6.4 was markedly less effective when perfused only during Ca(2+)-repletion. Ouabain (5 x 10(-6) M) had only a limited effect in exacerbating LDH leakage. Raising [K+]o significantly protected against LDH leakage, which fell to 36% at 16 mM [K+]. These features correspond with the Ca(2+)-paradox of the perfused rat heart an it is suggested that: (i) a Ca(2+)-paradox can be produced in the rat kidney; (ii) a similar mechanism governs the release of cytosolic proteins in these two preparations; and (iii) the damage mechanism of the plasmalemma is a transmembrane oxidoreductase-diaphorase molecular complex which generates H+ when activated by Ca(2+)-depletion.

Ultrastructural changes in rat kidney mitochondria in response to the oxygen- or calcium-paradox.

Isolated, perfused rat kidney released lactate dehydrogenase in response to the protocol of a standard oxygen-paradox or calcium-paradox. The results are comparable to those found with rat heart. The mitochondria of the proximal tubule cells at the end of the calcium-paradox were swollen, had mitochondrial bars and were subdivided with internal septa; after the oxygen-paradox they exhibited, in addition, many myelin figures. Such ultrastructural changes were characteristic of the mitochondria of skeletal and cardiac muscles damaged by a rise in [Ca2+]i. It is concluded (i) that typical calcium- and oxygen-paradoxes can be produced in kidney, (ii) that these are associated with a rise in [Ca2+]i and (iii) the proximal tubules, in particular, are damaged.

Comparison of maximal mid-expiratory flow, flow volume curves, and nitrogen closing volumes in patients with mild airway obstruction.

Maximal mid-expiratory flow (MMEF), maximal expiratory flow volume (MEFV) curves obtained with a wedge spirometer, and nitrogen closing volumes were determined in 38 patients with mild airway obstruction. Seventeen patients had asthma in remission and 21 had bronchitis. In all of them the forced expiratory volume in one second was within the normal range. Results were compared with predicted data in the literature and with a group of normal control subjects. In the patients with asthma, compared to predicted flow rates, MMEF was abnormal in 5, MEFV curves were abnormal in at least 8; closing volume was abnormally increased in only one patient, and an abnormal slope of the alveolar plateau was present in 4 additional patients. In the patients with bronchitis, compared to predicted flow rates, -MEF was reduced in 5, MEFV curves were abnormal in at least 7; increased closing volumes were present in 6, and the slope of the alveolar plateau was abnormal in 3 other patients. When flow rates were compared with those of normal control subjects, MMEF was about as frequently abnormal as MEFV curves, suggesting that the discrepancy between abnormal MMEF AND MEFV curves was due to variability of the predicted data. The results indicated that flow rates can be abnormal in subjects with normal closing volumes and a normal slope of the alveolar plateau, and that MEFV curves can be more sensitive than closing volume in detecting abnormalities in patients with mild airway obstruction. The results suggested that the use of both MEFV curves and the closing volume test for screening would defect functional abnormalities more frequently than either test alone.