Effects of weak electromagnetic fields on global electrocortical activity

Effects of weak electromagnetic fields are considered on recently proposed covariant and generalized coupling models of global electrocortical activity. A method to calculate the ratio of components of signal velocities is given. First-order shift in frequencies is obtained in the presence of a weak, time-varying magnetic field.     

GENETICS OF SORDARIA FIMICOLA. IV. LINKAGE GROUP I

El -Ani , Arif S., L. S. Olive , and Y. Kitani . (Columbia U., New York City.) Genetics of Sordaria fimicola. IV. Linkage group I. Amer. Jour. Bot. 48(8): 716–723. Illus. 1961.—A general technique for isolating and testing various morphological mutants induced by X ray is described. Eleven mutants differing in ascospore color, fertility, and rate and type of growth were studied in different crosses. This has led to the construction of the first linkage group in S. fimicola. The chromosome on which the 11 mutant loci occur is marked by a single locus on one arm and 10 on the opposite arm. The ascospore color mutant gray is autonomous, maintaining the mutant spore color in both homozygous and heterozygous asci, whereas milky, the other color mutant studied. expresses its mutant effect only in asci homozygous for the factor. Certain crosses involving 2 sterility mutants controlled by 2 non-allelic loci are fertile, and the progeny give rise to parentals as well as double-mutant and fertile recombinants.     

Carcinogen DNA adducts and the risk of colon cancer: case-control study

Colorectal cancer represents 8.5% of all tumours at the King Faisal Specialist Hospital & Research Centre. Environmental and dietary carcinogens such as polycyclic aromatic hydrocarbons (PAHs) and heterocyclic amines (HCAs) have long been suspected to play a prominent role in colon cancer aetiology. We designed a case-control study to test the hypothesis of whether or not the presence of DNA adducts can play a role in the aetiology of colon cancer. DNA adducts were measured in 24 cancerous and 20 non-cancerous tissue samples of newly diagnosed colon cancer patients by ³²P-post-labelling technique. Normal tissue from 19 hospital patients served as controls. The mean levels of adducts per 10¹⁰ nucleotides in cancerous and non-cancerous tissue were 151.75±217.27 and 114.81±186.10, respectively; however, only adducts in cancerous tissue were significantly higher than controls (32.78±57.51 per 10¹⁰ nucleotides) with p-values of 0.017. No BPDE-DNA adducts were found. No relationship was found between urinary cotinine as a marker of tobacco smoke and 1-hydroxypyrene as an indicator of an individual's internal dose of PAHs and DNA adducts. In a logistic regression model, only adducts in cancerous tissue were associated with the subsequent risk of colon cancer, with an odds ratio of 3.587 (95% confidence interval 0.833-15.448) after adjustment for age and the duration of living in the current region, but of a borderline significance (p=0.086). Although it is difficult to arrive at a definite conclusion from a small dataset, our preliminary results suggest the potential role of DNA adducts in the colon carcinogenesis process. Additional studies with larger sample sizes are needed to confirm our preliminary finding. It is also important to identify the structural characterization of these unknown DNA adducts in order to have a better understanding of whether or not environmental carcinogens play a role in the aetiology of colon cancer.