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The probe beam deflection technique, based on the mirage effect, has been applied to monitor laser processing of polymer and metal films and to measure damage thresholds of optical coatings. The technique is described and it will be shown that its sensitivity permits distinguishing between surface effects like heating and cracking, causing normal sound waves, and plasma formation outside the surface, giving rise to shockwaves. Examples are presented for single-shot ablation with 14 ns laser pulses of 248 nm wavelength. In particular, ablation studies of Ni films of varying thicknesses disclose a quantitative correlation between threshold fluences and thermal properties like heat diffusion, melting, and evaporation. In contrast, for Cr films a simple thermodynamic model fails because the films crack before melting and vaporizing.

The photoacoustic mirage effect technique was utilized to investigate excimer laser ablation of thin polymer (photoresist) and metal films. Layered systems, consisting of a photoresist-metal-SiO 2 structure, were ablated by KrF (λ = 248 nm) laser radiation at fluences up to 2 J/cm 2 . For the photoresist layer a linear dependence of the deflection amplitude on the etch rate was found in the low fluence regime (≤ 0.7 J/cm 2 ). Significant changes in the deflection signal occured when the ablation passed the interface between subsequent layers. This effect can be used to distinguish between different layers. Therefore, shock wave monitoring in principle offers the possibility for an in situ control of laser thin film processing. Selective ablation of metal films from the SiO 2 layer is limited to fluences below 2 J/cm 2 .

Epidemiological studies have shown a relationship between air pollution and allergic airway disease. In a previous study we have found that exposure to SO2 enhances allergic sensitization to inhaled ovalbumin (OA) in the guinea pig. We have now investigated the influence of pre-treatment with anti-inflammatory drugs on SO2-induced enhancement of allergic sensitization in this model. Four groups of 6 guinea pigs each were exposed to 5 ppm SO2 on 5 consecutive days over 8 h per day with intermittent inhalation of OA, while the air-control group was exposed to clean air and OA. During the period of SO2 exposure and sensitization three experimental groups were treated with indomethacin (group I), methylprednisolone (group M) and nebulized nedocromil sodium (group N), while the control group remained untreated. Guinea pigs were investigated for sensitization to OA by specific bronchial provocation tests using body plethysmographic measurement of compressed air (CA) and by measurement of specific antibody response in serum. While in the SO2-exposed control group 5 of 6 animals reacted to specific bronchial provocation testing (CA median 0.15 ml, range 0-0.175 ml), only 1 animal was sensitized in group M (CA 0 ml, 0–0.125, p 2 exposure inhibits SO2-induced enhancement of inhalative allergic sensitization in our guinea pig model.

Elevation of salivary SIgA-anti-casein has been shown to occur in newborn infants at risk of allergy. The present study was designed to follow 158 infants over 3 years to relate the onset of clinical disease to SIgA levels at birth. Newborn infants were divided into 3 groups according to their risk of allergy: Group I, (n= 62; no allergy risk); Group II, (n -30; low allergy risk); Group III (n= 66; high risk group). The groups were matched for smoking, social background, sex, and dietary habits of the patients. SIgA-anti-casein was determined by a direct ELIS A. During the first year 59 infants developed atopic diseases (n= 37 of Groups I and II; n= 22 of Group III). After 3 years 37/61 infants of the high risk group had developed allergic symptoms. The frequency of atopic disease correlated with increased salivary antibody titers at birth (p 250 EU/ml developed atopic symptoms at 1 year, 76% high risk infants with this titer developed atopic symptoms at 3 years of age. This study provides evidence that elevation of SIgA-anti-casein at birth not only reflects atopic risk as defined by cord blood IgE or family history, but correlates with the actual development of allergic disease during the first 3 years of life.

Secretory immunoglobulin A (SIgA) anti-casein and SIgA anti-beta-lactoglobulin (BLG) were determined in the saliva of 158 healthy mature infants at birth and in breast milk samples using a direct Elisa technique. IgG anti-casein and anti-BLG were measured in serum samples from mothers and newborns (cord blood). A high risk of allergy was defined in 66 infants who had cord blood (CB)-IgE levels greater than or equal to 0.9 IU/ml and/or parents with atopic diseases. Thirty infants had CB levels less than 0.9 IU/ml and parents without clinical symptoms of atopy but with elevated serum IgE concentrations or type I skin reactions to common allergens (low risk). Sixty-two infants had CB-IgE levels less than 0.9 IU/ml and healthy parents (no risk). The groups were matched for social status, smoking and dietary habits. SIgA anti-casein and anti-BLG were detected in all newborns. SIgA anti-casein was significantly higher (p less than 0.05) in high risk infants (medium 157; 50% confidence limits 45-270) than in no risk (48; 25-150) or low risk infants (43; 21-130). SIgA anti-casein values correlated with maternal allergy, maternal allergy plus CB-IgE, but not with paternal allergy. Breast milk SIgA anti-BLG was depressed (p less than 0.05) in mothers with manifest allergy compared to healthy mothers. Determination of salivary SIgA anti-casein may represent an additional screening method for early detection of infants with atopic disposition.

Salivary SIgA antibodies against RS virus were studied in 105 children during the first year of life. The infants were divided into groups according to their risk of atopy. At birth 13 neonates showed measurable amounts of SIgA to RS virus. In another 26 children specific antibodies were detected but in concentrations too low for quantitative analysis. During the first year of life this increased to 29 antibody-positive samples with measurable amounts of antibody and 39 with concentrations too low for quantitative determination. At this time 8 children of the high risk group had developed symptoms of allergy. None of these children had measurable amounts of SIgA anti-RSV in their saliva. In comparison, 10 of the remaining 26 high risk infants without symptoms of allergy did have such antibodies. Atopic infants had significantly more respiratory infections during the first year of life than nonatopic infants. The avidity of SIgA anti-RSV in neonatal samples was significantly higher than avidity determined in breast milk SIgA but comparable to the avidity of serum IgG. During the first year of life a continuing decrease of salivary SIgA avidity was observed.

Single-shot ablation thresholds of nickel and gold films in the thickness range from 50 nm to 7 μm have been measured for 14 ns laser pulses at 248 nm, using photoacoustic shock wave detection in air. The metal films were deposited on fused silica substrates. The ablation threshold was found to increase linearly with film thickness up to the thermal diffusion length of the film. Beyond this point it remains independent of film thickness. The proportionality between threshold fluence and thickness allows the prediction of ablation thresholds of metal films from the knowledge of their optical properties, evaporation enthalpies and thermal diffusivities. Physically it proves that ablation is driven by the energy density determined by the thermal diffusion length. A simple thermodynamic model describes the data well. Thermal diffusivities, an essential input for this model, were measured using the technique of transient thermal gratings. In addition, the substrate dependence of the ablation threshold was investigated for 150 nm Ni films.

Using photoacoustic shock wave detection and transient thermal gratings, ablation thresholds (at 248 nm) and thermal diffusivities of nickel and gold films on fused silica have been measured in air for thicknesses ranging from 50 nm to 7 μm. In addition, for a given film thickness, the substrate dependence of the ablation threshold was investigated. For films on fused silica, the ablation thresholds vary linearly with film thickness up to a certain value, determined by the thermal diffusion length of the metal. Beyond this point the thresholds are independent of film thickness. This proves that ablation is driven by the thermal energy deposited per volume, where the latter is made up by irradiated area times thermal diffusion length. A simple thermodynamic model describes the data and allows the prediction of ablation thresholds for bulk metals and metal films. Thermal diffusivity measurements show no distinct dependence on film thickness and reproduce within a certain margin the bulk values of the metal.

Excimer laser ablation of multi-layered films was studied using the photoacoustic mirage effect technique. Layered systems of a polymer-metal-SiO2 type was investigated for various metals between 0.5 and 2 J/cm2. Significant changes in the deflection signal were found when the ablation passed the interface between subsequent layers. This effect can be used to distinguish between different materials and is therefore suited for an in situ control of pulsed laser processing.© (1991) COPYRIGHT SPIE--The International Society for Optical Engineering. Downloading of the abstract is permitted for personal use only.

During multishot ablation with 248 nm excimer laser pulses for each single laser shot the shock wave emerging from the ablated material was monitored by the acoustic mirage effect. The shockwave parameters turned out to depend sensitively on the nature of the ablated material. In particular during ablation of a polymeric film/Si02/Si multilayer system distinct changes in the deflection signal were found when the ablation was driven through the interface between layers. Inspection by optical microscopy and depth profil ing was used as cross check. 1.

One hundred and fifty-eight healthy mature newborns were divided into 3 groups according to their risk of allergy: Group A, no risk (n = 62), group B, low risk (n = 30) and Group C, high risk (n = 66). Saliva was collected at birth and after 3 and 6 months. SIgA anti-casein and anti-beta-lactoglobulin were determined by a direct ELISA technique. The highest concentrations of secretory antibodies were measured after birth. After 3 months, breast fed infants had lower salivary SIgA anti-casein concentrations than the group receiving cow's milk (p less than 0.01). The effect of breast-feeding was seen even after a nursing period of only 3 weeks. Infants without risk of allergy fed cow's milk exclusively had higher SIgA anti-casein (p less than 0.03) and anti-beta-lactoglobulin concentrations than low risk infants at the age of 6 months. These data show a modifying effect of breast feeding on salivary SIgA production against cow's milk protein.

Local bronchial mucosal hypersensitivity following antigen feeding was studied in the guinea pig. Groups of 6 animals were fed 1% ovalbumin (OA) in tap water or tap water without antigen (control group) for different feeding periods (14, 28, 42, and 56 days). Inhalative provocations with increasing concentrations of OA (0.5–8% OA) were performed at the end of each feeding period followed by body plethysmographic measurement of airway obstruction. Specific bronchial hypersensitivity to inhaled OA was not found in the control group, whereas specific bronchial reactivity to OA, described as reactivity index, was significantly different from the control group after 14 (p