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The time-dependent response of a 1-[mm.sup.2] silicon photodiode was characterized by use of pulsed synchrotron radiation in the 4- to 16-nm-wavelength range. Modeling the input radiation pulse and the electrical response of the photodiode allowed the photodiode's capacitance as a function of wavelength and applied bias voltage to be determined. The capacitance was in the 7- to 19-pF range and resulted in response fall times as small as 0.4 ns. The capacitance determined by pulsed x-ray illumination was in good agreement with the capacitance determined by pulsed optical laser illumination. The absolute responsivity was measured by comparison with the responsivity of a calibrated photodiode. OCIS codes: 040.7480, 040.5160, 040.6040, 230.5170.

The responsivity of an extreme-ultraviolet transmission grating spectrometer with silicon photodiode detectors was measured with synchrotron radiation. The spectrometer was designed to record the absolute radiation flux in a wavelength bandpass centered at 30 nm. The transmission grating had a period of 200 nm and relatively high efficiencies in the +1 and the -1 diffraction orders that were dispersed on either side of the zero-order beam. Three photodiodes were positioned to measure the signals in the zero order and in the +1 and -1 orders. The photodiodes had aluminum overcoatings that passed the desired wavelength bandpass centered at 30 nm and attenuated higher-order radiation and wavelengths longer than approximately 80 nm. The spectrometer's responsivity, the ratio of the photodiode current to the incident radiation power, was determined as a function of the incident wavelength and the angle of the spectrometer with respect to the incident radiation beam. The spectrometer's responsivity was consistent with the product of the photodiode responsivity and the grating efficiency, both of which were separately measured while removed from the spectrometer. OCIS codes: 120.6200, 040.7480, 050.1950.

Histopathological and immunohistochemical studies were conducted to characterize vascular injuries in rats treated with phosphodiesterase (PDE) IV inhibitors SCH 351591 or SCH 534385. Sprague-Dawley rats were administered PDE IV inhibitors by gavage at a range of doses and times. The two PDE IV inhibitors induced comparable levels of vascular injury, primarily in the mesentery and to a lesser extent in the pancreas, kidney, liver, small intestine, and stomach. Mesenteric vascular changes occurred as early as one hour, progressively developed over twenty-four to forty-eight hours, peaked at seventy-two hours, and gradually subsided from seven to nine days. The typical morphology of the vascular toxicity consisted of hemorrhage and necrosis of arterioles and arteries, microvascular injury, fibrin deposition, and perivascular inflammation of a variety of blood vessels. The incidence and severity of mesenteric vascular injury increased in a time- and dose-dependent manner in SCH 351591- or SCH 534385- treated rats. Mesenteric vascular injury was frequently associated with activation of mast cells (MC), endothelial cells (EC), and macrophages (MØ). Immunohistochemical studies showed increases in CD63 immunoreactivity of mesenteric MC and in nitrotyrosine immunoreactivity of mesenteric EC and MØ. The present study also provides a morphological and cellular basis for evaluating candidate biomarkers of drug-induced vascular injury. [ABSTRACT FROM AUTHOR]

The present study was undertaken to characterize myocardial lesions in the rat induced by loWdoses of isoproterenol (Iso) and to correlate lesion severity with release of cardiac troponin T (cTnT) and changes in myocyte iNOS expression. Two types of cardiac injury patterns were observed. A Type I response, noted 3 or 6 hours postdosing with 8, 16, 32, or 64 µg/kg Iso, included potential reversible myocardial alterations associated with slight increases in serum cTnT (< 0.3 ng/mL) and a slight reduction in myocyte cTnT immunoreactivity. The second type of response noted 3, 6, 12, 24 or 48 hours postdosing with 125, 250, or 500 µg/kg Iso consisted of irreversible myocyte alterations, together with significant increases in serum cTnT (3–14 ng/mL) and a marked reduction of cTnT immunoreactivity. By 48 hours the hearts of rats dosed with 125–500 µg/kg Iso had developed interstitial fibrosis, and serum cTnT had declined to near control levels (0.06–0.18 ng/mL). Increases in iNOS immunoreactivity correlated with the lesion severity. These findings suggest that loWdoses of Iso exert complex effects on the myocardium and that the generation of NO through increased expression of iNOS could be an important factor in the pathogenesis of myocyte injury. [ABSTRACT FROM PUBLISHER]

States that the binding between the human immunodeficiency virus (HIV) surface protein, gp120, and the CD4 coreceptor is known to be initiated by electrostatic interactions. Ability of chlorpromazine to interact with proteins by charge transfer; Results of the testing of several derivatives for their ability to block binding of HIV to CD4... cells.