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Notes: We present results from a vacuum-ultraviolet (VUV) "photoabsorption imaging" technique based on the measurement of the time and space resolved absorption of a quasimonochromatic VUV beam from a laser plasma light source. The use of VUV radiation as a probe beam permits direct access to resonance lines of (singly and more highly charged) ions and also to the resonant and nonresonant continua of atoms and ions. In this experiment we have confined ourselves to measurements using the 3p–3d resonances of Ca, Ca+, and Ca2+ as markers of the temporal and spatial distribution of ground state atoms and ions in an expanding laser plasma plume. We show how time resolved column density maps may be extracted from such images. In addition we have extracted plasma plume velocities from the data, which compare well with an analytical laser ablation model. © 2000 American Institute of Physics.

Notes: The thermal oxidation of InP in dry oxygen has previously been shown to result in mixed oxide layers, even when grown at pressures as high as 500 atm. This appears to be caused by the slow diffusion of P and O2 through the oxide relative to In. This paper reports on the oxidation of InP in steam at one and 500 atm. Growth in one atm yields an oxide with a composition very similar to those grown in dry oxygen, indicating similar growth kinetics. However, at 500 atm of steam the growth kinetics are changed dramatically and result in a uniform InPO4 layer, suggesting that at high pressure, the H2O diffuses rapidly to the oxide-InP interface where the oxidation reaction occurs.

Notes: We have observed extreme-ultraviolet (XUV) "line-free" continuum emission from laser plasmas of high atomic number elements using targets irradiated with 248 nm laser pulses of 7 ps duration at a power density of ∼1013 W/cm2. Using both dispersive spectroscopy and streak camera detection, the spectral and temporal evolution of XUV continuum emission for several target atomic numbers has been measured on a time scale with an upper limit of several hundred picoseconds limited by amplified spontaneous emission. © 1997 American Institute of Physics.

Notes: In acute severe asthma, the earliest clinical effects of glucocorticosteroids occur from 4 to 5 h after systemic administration, but the mechanisms are unclear. In persistent asthma, corticosteroids are thought to suppress airway inflammation by modulating the expression of adhesion molecules, enzymes, and leucotactic cytokines, including granulocyte-macrophage colony stimulating factor (GM-CSF). GM-CSF is also overexpressed in the airways of symptomatic asthmatics.〈section xml:id="abs1-2"〉〈title type="main"〉ObjectivesTo examine the early effects of systemic corticosteroids on cytokine expression, we investigated whether ex vivo synthesis of GM-CSF is suppressed in the bronchoalveolar lavage (BAL) cells and peripheral blood mononuclear cells (PBMCs) of normal and mild allergic asthmatic subjects obtained 4 h after a single intravenous dose of prednisolone.〈section xml:id="abs1-3"〉〈title type="main"〉MethodsIn a randomized, double-blind, placebo-controlled study, BAL cells and PBMCs were obtained from mild atopic asthmatic patients (n = 9) and normal subjects (n = 9) 4 h after an intravenous bolus dose of 80 mg prednisolone, and cultured for 0–18 h in the presence or absence of lipopolysaccharide (LPS; 10 μg/mL). Enzyme immunoassay was used to assess GM-CSF levels in BAL cell and PBMC culture supernatants, and in BAL fluid.〈section xml:id="abs1-4"〉〈title type="main"〉ResultsAfter placebo, GM-CSF synthesis tended to be higher in BAL cells from asthmatics than in normals. LPS stimulation significantly increased median (interquartile range) GM-CSF synthesis by BAL cells ex vivo from 16.4 (23 to 74) to 35.8 (3–148) pg/106 cells in normals (P 〈 0.05), and from 59 (9 to 204) to 134 (24–288) pg/106 cells in asthmatics (P 〈 0.01). After intravenous prednisolone, the rise in GM-CSF production induced in BAL cells by LPS was completely abolished in both subject groups. In PBMCs of placebo-treated asthmatics (but not normals), LPS stimulated median GM-CSF synthesis from 164 (110 to 300) to 314 (235–485) pg/106 cells (P = 0.02), and this was blocked by intravenous prednisolone.〈section xml:id="abs1-5"〉〈title type="main"〉ConclusionsLPS-stimulated GM-CSF synthesis ex vivo is abolished in BAL cells of mild asthmatic and normal subjects, and in PBMCs of asthmatics, obtained 4 h after a single intravenous dose of prednisolone. Suppression of GM-CSF synthesis in airway and blood leucocytes may contribute to the early clinical efficacy of systemic glucocorticoids in acute allergic asthma.

Notes: The reproducibility of acute effects of inhaled PAF on airway calibre, circulating neutrophil count and any subsequent increase in bronchial responsiveness has been studied in six normal subjects and compared to the effects of inhaled lyso-PAF, the inactive precursor and metabolite of PAF. PAF caused acute bronchoconstriction and a transient fall in neutrophil count on two separate occasions in five out of six subjects (minimum percentage of baseline values (mean): first PAF challenge; sGaw 69%, V̇max30 72%; neutrophil count 70%; second PAF challenge; sGaw 61 %, V̇max30 74%, neutrophil count 63%). In one subject inhaled PAF caused bronchoconstriction and a transient fall in neutrophil count once, but a second challenge resulted in no detectable changes. There was no significant increase in bronchiai responsiveness to methacholine in any subject studied on five occasions over a 2-week period following each PAF challenge. Challenge with lyso-PAF did not cause acute effects or any subsequent changes in bronchial responsiveness. These findings demonstrate that any effects of inhaled PAF on bronchial responsiveness in normal man are small and probably not of clinical significance. It would also be inappropriate to use this human model to study the mechanisms of bronchial hyperresponsiveness or for the preliminary assessment of potential new anti-asthma drugs.

Notes: Sodium cromoglycate (SCG) has recently been formulated as a pressurized aerosol. Twenty-five asthmatic outpatients taking SCG via the Spinhaler were studied in a double-dummy, double-blind cross-over trial in which subjects took Spincaps containing 20 mg of SCG for 2 months, and for the alternate 2 months were treated with SCG aerosol delivering 1 mg/actuation.There was no evidence of clinical deterioration occurring during the period on aerosol SCG. During this period however cough frequency was significantly lower and when data for the 8-13 and 14-46 year age groups were analysed separately, this decrease was seen to be confined to the younger group. Furthermore, this group but not the adults, showed a significant improvement in morning peak expiratory flow rate.We conclude that the aerosol preparation of SCG is a useful alternative to delivery by Spinhaler for patients who are able to coordinate, and that it may have special advantages for children.

Notes: We have studied the effects of Ketotifen [Ke](10−4M and 10−6M) on two in vitro models of bronchoconstriction: actively sensitized guinea-pig trachea (GPT), and passively sensitized human bronchial muscle (HBM). Experiments were performed on matched pairs of tissues. Cumulative dose response curves [CDRC] for histamine and acetyl choline were constructed, and repeated after pre-incubation with Ke or saline control. The effect of Ke on maximal antigen induced contractions was also studied. Contraction of GPT by histamine and acetyl choline was inhibited by Ke 10−4M, though this effect was not apparent at high doses of acetyl choline. Ke 10−6M had a weaker inhibitory effect on histamine and acetyl choline induced responses. Contraction of GPT by antigen was unaffected by Ketotifen. In the HBM model. Ke 10−4M inhibited acetyl choline and antigen induced responses. Ketotifen, 10−6M had an inhibitory effect on acetyl choline induced contractions, though this was small, and not seen at higher agonist doses. Contraction of HBM by antigen was unaffected by Ke 10−6M. We were unable to obtain reproducible CD RC's to histamine with HBM. The weaker or absent effects of Ke 10−6M, a level close to that obtained in clinical practice, may explain some of the poor results of clinical trials, and suggest that efficacy may be improved by the use of higher doses.