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A study was done on the laser chemical vapor deposition of cobalt thin films. The nature of film growth was studied by comparing the initial growth rate on Suprasil quartz and soda lime glass and relating the growth rates to laser induced temperature as a function of thickness. It was shown that the crystal structure of the cobalt films is dependent on laser fluence. The hcp phase was produced by a fluence of 115 mJ cm(super -2) per pulse and the fcc phase was formed by higher fluences.

The exposure and emission limits of ICNIRP, IEC 60825-1 and ANSI Z136.1 to protect the skin are based on a limited number of in-vivo studies. To broaden the database, a computer model was developed to predict injury thresholds in the wavelength range from 400 nm to 20 µm and was validated by comparison with all applicable experimental threshold data (ED 50 ) in the wavelength range from 488 nm to 10.6 µm and exposure durations between 8 µs and 630 s. The model predictions compare favorably with the in-vivo data with an average ratio of computer prediction to ED 50 of 1.01 (standard deviation ± 46%) and a maximum deviation of 2.6. This computer model can be used to improve exposure limits or for a quantitative risk analysis of a given exposure of the skin., Competing Interests: The computer model described in this article is used – besides supporting the improvement of international safety limits – to predict skin injury thresholds as part of risk analysis studies for laser applications and products, offered by Seibersdorf Labor GmbH as commercial service., (© 2021 Optical Society of America under the terms of the OSA Open Access Publishing Agreement.)

The exposure and emission limits of ICNIRP, IEC 60825-1 and ANSI Z136.1 to protect the cornea are based on a limited number of in-vivo studies. To broaden the database, a computer model was developed to predict injury thresholds in the wavelength range from 1050 nm to 10.6 µm and was validated by comparison with all applicable experimental threshold data (ED 50 ) with exposure duration between 1.7 ns and 100 s. The model predictions compare favorably with the in-vivo data with an average ratio of computer prediction to ED 50 of 0.94 (standard deviation ± 30%) and a maximum deviation of less than 2. This computer model can be used to improve exposure limits or for a quantitative risk analysis of a given exposure of the cornea., Competing Interests: The computer model described in this article is used – besides supporting the improvement of international safety limits – to predict corneal injury threshold for risk analysis studies for laser applications and products, offered by Seibersdorf Labor GmbH as commercial service. The co-authors Bruce E. Stuck and David J. Lund have no relevant financial interests in this article and no potential conflicts of interest to disclose., (© 2020 Optical Society of America under the terms of the OSA Open Access Publishing Agreement.)

Purpose: To investigate whether infrared radiation (IRR)-induced cataract is instant or is associated with a time delay between the exposure and the onset of lens light scattering after an exposure to just above threshold dose., Methods: Six-weeks-old albino Sprague-Dawley female rats were unilaterally exposed to 197 W/cm2 IRR at 1090 nm within the dilated pupil. In the first experiment, the animals were exposed with four exposure times of 5, 8, 13 and 20 second, respectively. At 24 hr after exposure, the light scattering in both exposed and contralateral not exposed lenses was measured. Based on the first experiment, four postexposure time groups were exposed unilaterally to 1090 nm IRR of 197 W/cm2 for 8 second. At 6, 18, 55 and 168 hr after exposure, the light scattering in both lenses was measured., Results: A 197 W/cm2 IRR-induced light scattering in the lens with exposures of at least 8 second. Further, after exposure to IRR of 197 W/cm2 for 8 second, the light-scattering increase in the lens was delayed approximately 16 hr after the exposure., Conclusion: There is a time delay between the exposure and the onset of cataract after exposure to close to threshold dose implicating that either near IRR cataract is photochemical or there is a time delay in the biological expression of thermally induced damage., (© 2014 Acta Ophthalmologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.)

The damage mechanism for near-infrared radiation (IRR) induced cataract is unclear. Both a photochemical and a thermal mechanism were suggested. The current paper aims to elucidate a photochemical effect based on investigation of irradiance-exposure time reciprocity. Groups of 20 rats were unilaterally exposed to 96-W/cm(2) IRR at 1090 nm within the dilated pupil accumulating 57, 103, 198, and 344 kJ/cm(2), respectively. Temperature was recorded at the limbus of the exposed eye. Seven days after exposure, the lenses were macroscopically imaged and light scattering was quantitatively measured. The average maximum temperature increases for exposure times of 10, 18, 33, and 60 min were expressed as 7.0 ± 1.1, 6.8 ± 1.1, 7.6 ± 1.3, and 7.4 ± 1.1 °C [CI (0.95)] at the limbus of the exposed eye. The difference of light scattering in the lenses between exposed and contralateral not-exposed eyes was 0.00 ± 0.02, 0.01 ± 0.03, -0.01 ± 0.02, and -0.01 ± 0.03 transformed equivalent diazepam concentration (tEDC), respectively, and no apparent morphological changes in the lens were observed. An exposure to 96-W/cm(2) 1090-nm IRR projected on the cornea within the dilated pupil accumulating radiant exposures up to 344 kJ/cm(2) does not induce cataract if the temperature rise at the limbus is <8 °C. This is consistent with a thermal damage mechanism for IRR-induced cataract.

An in vivo exposure to 197  W/cm 2 1090-nm infrared radiation (IRR) requires a minimum 8 s for cataract induction. The present study aims to determine the ocular temperature evolution and the associated heat flow at the same exposure conditions. Two groups of 12 rats were unilaterally exposed within the dilated pupil with a close to collimated beam between lens and retina. Temperature was recorded with thermocouples. Within 5 min after exposure, the lens light scattering was measured. In one group, the temperature rise in the exposed eye, expressed as a confidence interval (0.95), was 11±3°C at the limbus, 16±6°C in the vitreous behind lens, and 16±7°C on the sclera next to the optic nerve, respectively. In the other group, the temperature rise in the exposed eye was 9±1°C at the limbus and 26±11°C on the sclera next to the optic nerve, respectively. The difference of forward light scattering between exposed and contralateral not exposed eye was 0.01±0.09 tEDC. An exposure to 197  W/cm 2 1090-nm IRR for 8 s induces a temperature increase of 10°C at the limbus and 26°C close to the retina. IRR cataract is probably of thermal origin.

Exposure limits (ELs) for laser and optical broadband radiation that are derived to protect the retina from adverse thermally-induced effects vary as a function of wavelength, exposure duration, and retinal irradiance diameter (spot size) expressed as the angular subtense α. A review of ex vivo injury threshold data shows that, in the ns regime, the microcavitation-induced damage mechanism results in retinal injury thresholds below thermal denaturation-induced thresholds. This appears to be the reason that the injury thresholds for retinal spot sizes of about 80 μm (α = 6 mrad) and pulse durations of about 5 ns in the green wavelength range are very close to current ELs, calling for a reduction of the EL in the ns regime. The ELs, expressed in terms of retinal radiant exposure or radiance dose, currently exhibit a 1/α dependence up to a retinal spot size of 100 mrad, referred to as αmax. For α ≥ αmax, the EL is a constant retinal radiant exposure (no α dependence) for any given exposure duration. Recent ex vivo, computer model, and non-human primate in vivo threshold data provide a more complete assessment of the retinal irradiance diameter dependence for a wide range of exposure durations. The transition of the 1/α dependence to a constant retinal radiant exposure (or constant radiance dose) is not a constant αmax but varies as a function of the exposure duration. The value of αmax of 100 mrad reflects the spot size dependence of the injury thresholds only for longer duration exposures. The injury threshold data suggest that αmax could increase as a function of the exposure duration, starting in the range of 5 mrad in the μs regime, which would increase the EL for pulsed exposure and extended sources by up to a factor of 20, while still assuring an appropriate reduction factor between the injury threshold and the exposure limit.

Background: Recent studies suggest that ultraviolet (UV) A1 phototherapy is an effective treatment for localized scleroderma (LS); however, the optimum UVA1 dose remains to be determined., Objective: We sought to compare the immediate and long-term efficacy of low- versus medium-dose UVA1 phototherapy for plaque-type LS., Methods: Three comparable plaques in 16 patients were treated with 20 J/cm2 UVA1, 70 J/cm2 UVA1, or no irradiation. In total, 30 treatments were given. Skin thickness was determined by high-frequency ultrasound examination and clinical scoring. Assessments were done at baseline, immediately after treatment, and 3, 6, and 12 months thereafter., Results: Ultrasound measurement showed a significantly greater reduction of skin thickness with 70 J/cm2 than with 20 J/cm2 at all time points of the study except immediately after UVA1 treatment. The clinical score of the irradiated plaques also decreased substantially but failed to detect a significant difference between the two dose regimens., Limitations: Our results only pertain to plaque-type LS and are limited by a small sample size., Conclusion: Medium-dose provides for better long-term results than low-dose UVA1 in LS as shown by ultrasound assessment. With clinical scoring, no significant difference between the two UVA1 dose regimens was detected, indicating that ultrasound measurement is a more sensitive method for quantifying treatment-induced skin changes in patients with LS.

Excised bovine eyes are used as models for threshold determination of 532-nm laser-induced thermal damage of the retina in the pulse duration regime of 100 micros to 2 s for varying laser spot size diameters. The thresholds as determined by fluorescence viability staining compare well with the prediction of an extended Thompson-Gerstman computer model. Both models compare well with published Rhesus monkey threshold data. A previously unknown variation of the spot size dependence is seen for different pulse durations, which allows for a more complete understanding of the retinal thermal damage. Current International Commission on Nonionized Radiation Protection (ICNIRP), American National Standards Institute (ANS), and International Electromechanical Commission (IEC) laser and incoherent optical radiation exposure limits can be increased for extended sources for pulsed exposures. We conclude that the damage mechanism at threshold detected at 24 and 1 h for the nonhuman primate model is retinal pigment epithelium (RPE) cell damage and not thermal coagulation of the sensory retina. This work validates the bovine ex vivo and computer models for prediction of thresholds of thermally induced damage in the time domain of 10 micros to 2 s, which provides the basis for safety analysis of more complicated retinal exposure scenarios such as repetitive pulses, nonconstant retinal irradiance profiles, and scanned exposure.

The acceptance and usability of personal protection against solar UV radiation was evaluated in a field study with a group of tinsmiths in Austria. The personal protective measures (PPM) tested involved four categories: shirts, headwear, sunglasses and topically applied sunscreens; at least six different products per category were tested. Recommendations for the "ideal" shirt, headwear, pair of sunglasses and topical sunscreen are given based on data from questionnaires, i.e., from the point of view of the workers, independently from the actual physical level of protection (such as low transmittance or area of coverage) provided. It is argued that in practice it is important to consider the acceptance and usability of protective measures as well as the level of physical protection when providing PPM.

The retinal injury threshold dose for laser exposure varies as a function of the irradiated area on the retina. Zuclich reported thresholds for laser-induced retinal injury from 532 nm, nanosecond-duration laser exposures that varied as the square of the diameter of the irradiated area on the retina. We report data for 0.1-s-duration retinal exposures to 514-nm, argon laser irradiation. Thresholds for macular injury at 24 h are 1.05, 1.40, 1.77, 3.58, 8.60, and 18.6 mJ for retinal exposures at irradiance diameters of 20, 69, 136, 281, 562, and 1081 microm, respectively. These thresholds vary as the diameter of the irradiated retinal area. The relationship between the retinal injury threshold and retinal irradiance diameter is a function of the exposure duration. The 0.1-s-duration data of this experiment and the nanosecond-duration data of Zuclich show that the ED(50) (50% effective dose) for exposure to a highly collimated beam does not decrease relative to the value obtained for a retinal irradiance diameter of 100 microm. These results can form the basis to improve current laser safety guidelines in the nanosecond-duration regime. These results are relevant for ophthalmic devices incorporating both wavefront correction and retinal exposure to a collimated laser.

Context: Despite growing support for melatonin as a promising agent for cancer treatment and possibly cancer prevention, few studies have elucidated factors that influence endogenous melatonin. This overview summarizes dietary and lifestyle factors that have been shown to affect circulating melatonin levels., Biological Mechanisms: To date, many animal studies and in vitro experiments have illustrated that melatonin possesses oncostatic activity. Mechanisms that are currently being studied include melatonin's activity as an indirect antioxidant and free radical scavenger; its action on the immune system; suppression of fatty acid uptake and metabolism; and its ability to increase the degradation of calmoduline and to induce apoptosis. Studies further suggest that melatonin reduces local estrogen synthesis, through down-regulation of the hypothalamic-pituitary reproductive axis and direct actions of melatonin at the tumor cell level, thus behaving as a SERM., Therapeutic Applications: Several small clinical trials have demonstrated that melatonin has some potential, either alone or in combination with standard cancer therapy, to yield favorable responses. Melatonin or its precursor tryptophan have been found in numerous edible plants, but more studies are needed to evaluate the influence of diets rich in tryptophan and melatonin on circulating melatonin levels in humans. Age, BMI, parity, and the use of certain drugs remain the factors that have been associated most consistently with aMT6s levels., Discussion: Further insights into the effects of dietary and lifestyle factors that modulate circulating melatonin levels may provide the basis for novel interventions to exploit melatonin for the prevention and treatment of human diseases.

In order to evaluate the potential hazard for the skin and the eye presented by solar ultraviolet radiation, and to take appropriate precautions, it is necessary to characterise the biological effective irradiance or dose. Recently, inexpensive UV indicator cards became available that in principle would provide an attractive means to roughly indicate the local level of erythemal solar UV irradiance. We have characterised the properties of a number of different types of UV indicator cards. Several parameters which may influence the colour of the cards were examined with both outdoor trials under solar UV as well as indoor trials using a filtered xenon arc lamp. Our findings show that the tested cards do not give an appropriate estimation of the effective irradiance due to their spectral sensitivity and their temperature dependence. The application area of the tested UV indicator cards is therefore limited to certain temperature ranges and to seasons where a certain ratio between solar UV-A and solar UV-B occurs.

While the mutagenic and carcinogenic properties of longwave UV light (UVA) are well established, mechanisms of UVA mutagenesis remain a matter of debate. To elucidate the mechanisms of mutation formation with UVA in human skin, we determined the spectra of UVA- and UVB-induced mutations in primary human fibroblasts. As with UVB, we found the majority of mutations to be C-to-T transitions also with UVA. For both UVA and UVB, these transitions were found within runs of pyrimidines, at identical hotspots, and with the same predilection for the nontranscribed strand. They also included CC-to-TT tandem mutations. Therefore, these mutations point to a major role of pyrimidine dimers not only in UVB but also in UVA mutagenesis. While some differences were noted, the similarity between the spectra of UVA- and UVB-induced mutations further supports similar mechanisms of mutation formation. A non-dimer type of DNA damage does not appear to play a major role in either UVA or UVB mutagenesis. Therefore, the previously reported increasing mutagenicity per dimer with increasing wavelengths cannot be due to non-dimer DNA damage. Differences in the cellular response to UVA and UVB, such as the less prominent activation of p53 by UVA, might determine a different mutagenic outcome of UVA- and UVB-induced dimers.

Environmental lighting powerfully suppresses the physiologic release of melatonin, which typically peaks in the middle of the night. This decreased melatonin production has been hypothesized to increase the risk of cancer. Evidence from experimental studies supports a link between melatonin and tumor growth. There is also fairly consistent indirect evidence from observational studies for an association between melatonin suppression, using night work as a surrogate, and breast cancer risk.

The derivations of human exposure limits for laser radiation rely heavily upon experimental ocular injury studies. The limits are derived by committees of ophthalmic experts through a review of all available threshold data and an understanding of mechanisms of laser/tissue interaction. A major point of discussion in this derivation process relates to the level of uncertainty of the threshold of injury. An indication of the level of uncertainty relates to the slope of the transformed dose-response curve, or the "probit plot" of the data. The most cited point on the probit plot is the exposure that represents a 50% probability of injury: the ED-50. This value is frequently referred to as the "threshold," even though some experimental damage points exist below this "threshold." An analysis of any number of example data sets reveals that the slope in most experiments cannot be explained by biological variation alone. The optical, thermophysical, and biological factors influencing the probit plot are critically analyzed to provide guidance for deriving exposure limits. By theoretically modeling an experiment, small errors in focus are shown to produce a substantial change in the ED-50 and the slope of the probit plot.

Leukotriene C4 (LTC4) contracts isolated bullfrog lung. This study examined effects of cold-acclimation and the involvement of extracellular and intracellular Ca++ on the contractile response to LTC4. The response to LTC4 was greater in lungs from warm-acclimated (22 degrees C) frogs compared with cold-acclimated (5 degrees C) frogs at incubation temperatures of both 22 degrees C and 5 degrees C. LTC4, LTC5, and N-methyl LTC4 were equally effective in stimulating lung contraction at concentrations from 1-100 nM. Nicardipine (3 microM) partially antagonized the response to LTC4, but verapamil, nifedipine, or nitrendipine at the same concentration was ineffective. Ethylene glycol tetraacetic acid (EGTA, 0.3 mM) prevented the response to 30 nM LTC4, but the response was restored when the lung was retested in EGTA-free medium containing Ca++, suggesting that extracellular Ca++ was involved in the response. Caffeine (10 mM) or thapsigargin (1 mM) inhibited the responses to LTC4, suggesting a role for intracellular Ca++ in the contraction.