Abstract— Stationary cells of isogenic pairs of Escherichia coli K12 strains presumably differing only in the recA function have been inactivated with near‐UV (300–400 nm) radiation. Based on near‐UV inactivation kinetics, the strains can be divided into two discrete categories in which near‐UV sensitivity does not necessarily correlate with far‐UV sensitivity conferred by two different recA alleles. Lack of overlap between near‐UV and far‐UV (recA) sensitivity can be explained hy assuming that a different chromosomal gene (nur) controls near‐UV sensitivity. Support for this hypothesis comes from a mating experiment in which four selected recombinants, isogenic with respect to auxotrophic markers, were identified exhibiting all four possible combinations of far‐UV (recA1 vs recA +) and near‐UV sensitivity (nur vs nur+). Transduction with phase P1 has shown that introduction of the recA1 allele into a recA+ recipient does not affect the near‐UV sensitivity of the recipient. Additional matings together with transduction experiments suggest that the nur gene is located at a position on the E. coli linkage map clearly separable from recA (minute 58).

No abstract

No abstract

A 28-year-old male with hepatic actinomycosis presented with several months of anorexia, weight loss, fever, night sweats, and mild right upper quadrant abdominal tenderness. Despite normal liver function tests, hepatic involvement was demonstrated by imaging studies. A liver biopsy and ultrasound-guided aspirate were, however, unrewarding. Laparotomy was, therefore, necessary to establish a definitive diagnosis. The patients was then successfully treated with intravenous penicillin followed by oral clindamycin. This case is presented to illustrate the diagnostic difficulties that may be encountered in such patients with hepatic actinomycosis.