Mefodiy Romanowski. Biological and medical researcher 1868-1911. An episode in the fight against tuberculosis.

Mefodiy Romanowski, a country doctor in tsarist Ukraine, developed a perspicacious interest in cell biology as a basic requirement for the study of physiology and pathology. He went on to characterize tuberculosis as a disease whose pathogens disrupted the phospho-proteins of the cell nucleus. This led to his concocting a melange of acidic phosphorus compounds, under the trade name Phosphacid, as a remedy (to be injected subcutaneously). He and others claimed a measure of success for the treatment; it was approved by the Russian Council of Physicians; and despite revolution and war it enjoyed esteem in Eastern Europe for over three decades after Romanowski's early death in 1911. Its last known manufactory, in Warsaw, was destroyed during the 1944 Uprising.

A kinetic analysis of spontaneous rho- mutations in yeast.

Spontaneous mutation to the petite state at the level of the individual cell was studied in a haploid strain of yeast by the technique of pedigree analysis. Results indicated that (1) the mutability of rho+ cells within a population in log phase is variable; (2) rho+ mitotic buds are, on the average, about 50% more mutable than the rho+ cells from which they arose; (3) the mutability of a rho+ cell tends to decrease as it produces consecutive buds: (4) the probability that a mother cell will become rho- at or immediately subsequent to cell division is, on the average, one third the probability that its bud will be rho-; (5) most, if not all spontaneous rho- mutant cells contain mitochondrial DNA as judged from suppressiveness measurements. The data indicate that the spontaneous production of a mutant cell is a multi-step process. Neither a replicative advantage of defective mitochondrial DNA nor the existence of a "master" mitochondrial genome provides a satisfactory explanation of the process. Either selective dispensation of defective mitochondria to the bud at cytokinesis or normal retention by the mother cell of factors influencing the amplification or rate of induction of defective mitochondrial DNA could be involved.