Lack of asbestos contamination of paraffin

OBJECTIVE: To investigate possible asbestos contamination of paraffin and migration by asbestos fibers during the tissue-embedding process. DESIGN: Three sample categories were included in the study: (1) commercially available paraffin samples; (2) procedural control samples, which were prepared by processing the paraffin through the use of standard solvents and instruments; and (3) samples taken from areas adjacent to embedded tissue and evaluated for migration of asbestos from the tissue into the surrounding paraffin. The analysis of collected material from all samples was performed with analytical transmission electron microscopy. RESULTS: Only one extremely small tremolite fiber was found in any of the commercially available samples of paraffin. No asbestos fibers were found either in the procedural control samples or in the samples taken adjacent to the embedded lung tissue. CONCLUSIONS: First, it was extremely unlikely that any of the commercial paraffin samples would have skewed data due to embedded tissue. Second, the processing and instrumentation was not found to contribute asbestos material to the paraffin during the preparations. Finally, embedded tissue that contained high numbers of fibers, both uncoated fibers and asbestos bodies, did not contribute asbestos to the adjacent paraffin.     

On an implementation of standard bases and syzygies in SINGULAR

We describe an implementation of a general standard basis algorithm, valid for any monomial ordering compatible with the natural semigroup structure. We concentrate on new strategies which have proved useful, in particular in the non-wellordering case. Moreover, we describe the first implementation of Schreyer's method to compute syzygies and compare it with other, more classical methods. Comparisons of the computing time of several examples in the system SINGULAR give hints as to which strategies should be used in different classes of examples.     

Genetic, cytogenetic, and carcinogenic effects of radon: a review

Radon exposure has been linked to lung carcinogenesis in both human and animal studies. Studies of smoking and nonsmoking uranium miners indicate that radon alone is a risk factor for lung cancer at the levels encountered by these miners, although the possibility exists that other substances in the mine environment affect the radon-induced response. The relevance of data from mines to the lower-exposure home environment is often questioned; still, a recent study of miners exposed to relatively low radon concentrations demonstrated a statistically significant increase for lung and laryngeal cancer deaths. In two major series of experiments with rats, the primary carcinogenic effect found was respiratory tract tumors, and evidence for an inverse exposure-rate effect was also noted. Although this inverse dose-rate effect also has been described in underground miner studies, it may not similarly apply to radon in the home environment. This observation is due to the fact that, below a certain exposure, cells are hit once or not at all, and one would not expect any dose-rate effect, either normal or inverse. Because some chromosome aberrations persist in cycling cells as stable events, cytogenetic studies with radon are being performed to help complete the understanding of the events leading to radon-induced neoplasia. Radon has been found to induce 13 times as much cytogenetic damage (as measured by the occurrence of micronuclei) than a similar dose of 60Co. A wide variety of mutation systems have demonstrated alpha-particle mutagenesis; recent investigations have focused on the molecular basis of alpha-induced mutagenesis. Gene mutations are induced by radon in a linear and dose-dependent fashion, and with a high biological effect relative to low-LET irradiation. Studies of the hprt locus show that approximately half of the alpha-induced mutations arise by complete deletion of the gene; the remaining mutations are split between partial deletions, rearrangements, and events not detectable by Southern blot or PCR exon analysis. Although other mutation systems do not show the same spectra as observed in the hprt gene (suggesting that the gene environment affects response), DNA deletions or multilocus lesions of various size appear to be predominant after radon exposure. As data emerge regarding radon-induced changes at the chromosomal and molecular level, the mechanisms involved in radon carcinogenesis are being clarified. This information should increase the understanding of risk at the low exposure levels typically found in the home.     

Absence of contour linking in peripheral vision

Human foveal vision is subserved initially by groups of spatial, temporal and orientational 'filters', the outputs of which are combined to define perceptual objects. Although a great deal is known about the filtering properties of individual cortical cells, relatively little is known about the nature of this 'linking' process. One recent approach has shown that the process can be thought of in terms of an association field whose strength is determined conjointly by the orientation and distance of the object. Here we describe a fundamental difference in this feature-linking process in central and peripheral parts of the visual field, which provides insight into the ways that foveal and peripheral visual perception differ. In the fovea, performance can be explained only by intercellular linking operations whereas in the periphery intracellular filtering will suffice. This difference represents a substantial economy in cortical neuronal processing of peripheral visual information and may allow a recent theory of intercellular binding to be tested.