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Biomedical subjects

W Scheid

Publications and source records attributed to W Scheid.

At least 19 recordsLinked to original sources
PubMed2001

Fifth-order corrected field descriptions of the Hermite-Gaussian (0,0) and (0,1) mode laser beam.

In this paper, we extend the work of Barton and Alexander [J. App. Phys. 66, 2800 (1989)] on the fifth-order corrected field expressions for a Hermite-Gaussian (0,0) mode laser beam to more general cases with adjustable parameters. The parametric dependence of the electron dynamics is investigated by numerical methods. Finally, the fifth-order corrected field equations for the Hermite-Gaussian (0,1) mode are also presented.

Journal Article↗
PubMed1997

Fluence and mutagenic side effects of excimer laser radiation applied in ophthalmology in human lymphocytes in vitro.

PURPOSE: To investigate the influence of different fluences in 193 and 248 nm excimer laser radiation on the yields of chromatid and chromosome aberrations induced in human lymphocytes in vitro. METHOD: Heparinized human blood was exposed to 193 or 248 nm excimer laser radiation. The fluence was gradually increased from 21 to 400 mJ/cm2 in 193 nm (constant total energy of 250 J) and from 150 to 377 mJ/cm2 in 248 nm radiation (constant total energy of 500 J). Chromatid and chromosome aberrations were then analysed microscopically. RESULTS: The yields of chromatid breaks and achromatic lesions depend on the fluence per pulse. This dependence contains a linear component, indicating a threshold of about 70 mJ/cm2 fluence in 193 nm and of about 250 mJ/cm2 fluence in 248 nm laser radiation. An increase of the yield of dicentric chromosomes could only be observed at the highest fluence tested (377 mJ/cm2) in the 248 nm series. Over 126 mJ/cm2 in 193 nm radiation no lymphocytes could be cultured and therefore no aberrations could be found. CONCLUSIONS: Our findings show that the fluence of 193 nm and of 248 nm excimer laser radiation has an effect on the yields of chromatid breaks and achromatic lesions in human lymphocytes under in vitro conditions.

Adult↗
PubMed1995

Biological dosimetry after extensive diagnostic x-ray exposure.

The yield of chromosome aberrations (dicentric and ring chromosomes) was determined for five patients who had been extensively exposed to diagnostic x rays. Remarkably high aberration yields were obtained for each of them leading to correspondingly high equivalent whole body doses ("biological dosimetry"). The contribution of iodized contrast media and computing tomography to the biologically estimated doses is discussed.

Adult↗
PubMed1993

[Calcium antagonists as amplifiers of the mutagenicity of cytostatic drugs].

Some calcium antagonists enhance synergistically the mutagenic efficiency of cytostatics. The results so far obtained concerning this phenomenon are described and discussed: (1) chromosome aberrations induced (in vitro) in human lymphocytes (cytostatics; bleomycin and peplomycin; calcium antagonists: verapamil and fendiline), (2) chromosome and chromatid aberrations induced (in vitro) in Chinese hamster ovary (CHO) cells (cytostatic: mitomycin C; calcium antagonist: verapamil), (3) gene mutations induced in the bacterium Salmonella typhimurium (cytostatics: mainly various anilinoacridine drugs; calcium antagonist: verapamil). In all 3 studies neither verapamil nor fendiline proved to be mutagenic when applied alone. The "comutagenicity" of calcium antagonists is compared with the enhancement of the cytotoxic (cell killing) efficiency of cytostatics by calcium antagonists. Both phenomena--potentiation of mutagenicity and of cytotoxicity--are interpreted on the basis of the "accumulation hypothesis". According to this hypothesis those calcium antagonists would enhance the mutagenic and cytotoxic efficiency of the cytostatics by inhibiting their extrusion from the cell. Consequently, the cytostatics would be accumulated in the cell and this would increase their mutagenic and cytotoxic efficiency. Since not all calcium antagonists investigated so far enhance the mutagenicity and cytotoxicity of cytostatics, this potentiation seems not to be caused by their calcium antagonistic action per se. Molecular, evolutionary, and medical aspects of the "accumulation hypothesis" are shortly discussed.

Animals↗