Mutator is a powerful system for generating new mutants in maize. Mutator activity is attributable to a family of transposable, multicopy Mu elements, but none of the known elements is an autonomous (regulatory) element. This paper reports the discovery of Mu9, a 4942-base-pair Mu element that was cloned after it transposed into the Bronze-2 locus.

In the progeny of an active Mutator plant, the number of Mu elements increases on self-pollination and maintains the average parental Mu content on outcrossing to a non-Mutator line; both patterns of transmission require an increase in the absolute number of Mu elements from one generation to the next. The same average copy number of Mu elements is transmitted through the male and female, but there is wide variation in the absolute copy number among the progeny. In inactive Mutator plants-defined both by the loss of somatic instability at a reporter gene (bronze2-mu1) and by modification of the HinfI sites in the terminal inverted repeat sequences of Mu elements - the absolute copy number of Mu elements is fixed in the parent. Thus, in outcrosses Mu element number is halved, and on self-pollination Mu copy number is constant. Reactivation of somatic mutability at cryptic bz2-mu1 alleles in inactive individuals by crossing to an active line seems not to involve an increase in Mu element copy number transmitted by the inactive individual. These and other results suggest that increases in Mu copy number occur late in plant development or in the gametophyte rather than after fertilization.

The in vitro activity of Ro 13-9904 was assessed against clinical isolates of common bacteria. Its activity against most enterobacteria was similar to that of cefotaxime and moxalactam, but it was even more active than these compounds against all Proteus species. It was also highly active against Haemophilus influenzae and Neisseria gonorrhoeae, including /3-lactamase producers. Like Fig. 1) MICs and MBCs. Minimal inhibitory concentrations (MICs) were determined by agar dilution as described before (1). Unless otherwise stated, the inoculum consisted of about 104 colony-forming units (CFU) except for staphylococci, for which we report results obtained with an inoculum of 106 CFU. The medium used was diagnostic sensitivity test agar (Oxoid CM 261). This was supplemented with 6% saponinlysed horse blood for anaerobes, streptococci (except Streptococcus faecalis), Haemophius inflenzae, and Neisseria gonorrhoeae. Incubation was in air except for streptococci (other than S. faecalis), H. influenzae, and N. gonorrhoeae, which were incubated in 10% carbon dioxide, and anaerobes, which were incubated in 80% nitrogen-10% hydrogen-10% carbon dioxide. Results were read after 18 to 24 h except for anaerobes, which were read after about 40 h. The inoculum was prepared by dilution of an overnight culture in nutrient broth except for anaerobes, alpha-and nonhemolytic streptococci, and Streptococcus pneumoniae, for which bacterial growth was scraped off Columbia agar (Oxoid CM 331) containing 6% horse blood (blood agar), and H. influenzae and N. gonorrhoeae, for which bacterial growth was scraped off diagnostic sensitivity test agar containing 6% lysed horse blood.We also determined MICs and minimal bactericidal concentrations (MBCs) for some organisms by broth dilution in Iso-Sensitest broth (Oxoid CM 473

The in vitro activity of norfloxacin (MK-0366) compared with that of 1-lactam antibiotics and, where appropriate, of gentamicin or metronidazole was assessed against recent clinical isolates of common bacteria. The compound was highly active against most enterobacteria (minimal inhibitory concentrations [MICs], 0.008 to 32 ,ubg/ml; 90% inhibited by 0.25 ,ug/ml), Haemophilus influenzae (MICs, 0.03 to 0.12 ,ug/ml), and Neisseria gonorrhoeae (MICs, 0.008 to 0.016 jig/ml). It was also active against Pseudomonas aeruginosa (MICs, 0.12 to 2 ,g/ml), most other pseudomonads (MICs, 0.03 to 32 ,ug/ml), and Acinetobacter calcoaceticus (MICs, 0.06 to 4 ,ug/ml). Norfloxacin was somewhat less active against staphylococci (MICs, 0.25 to 4 ,ug/ml; 1 ,ug/ml required to inhibit 50o of isolates) and streptococci (MICs, 0.5 to 64 jxg/ml). Members of the Bacteroidesfragilis group of anaerobes were relatively resistant to norfloxacin (MICs, 8 to 128 ,ug/ml), as were most other anaerobes.

The in-vitro antibacterial activity of ceftazidime was assessed against recent clinical isolates of common bacteria and also against reference strains that produced known beta-lactamases. The compound was active, though less so than cephaloridine against staphylococci and streptococci with MICs mostly 0.12-2 mg/l for streptococci and 8 mg/l for staphylococci, but enterococci (MICs > or =64 mg/l) and methicillin-resistant staphylococci (MICs 16-32 mg/l) were resistant. Penicillin-resistant pneumococci (MICs 2-4 mg/l) were much less sensitive than other pneumococci (MICs 0.12-0.25 mg/l). Ceftazidime was also active, but slightly less so than cefotaxime or moxalactam, against enterobacteria (MICs mostly 0.12-0.25 mg/l). Its activity was also inferior to that of cefotaxime against Neisseria gonorrhoeae (MICs mostly 0.03-0.06 mg/l) and Haemophilus influenzae (MICs mostly 0.06-0.25 mg/l). However it was about eightfold more active than cefotaxime or moxalactam against Pseudomonas aeruginosa (MICs mostly 1-4 mg/l), and it was also more active than these compounds against other pseudomonads. Ceftazidime was less active than cefoxitin against Bacteroides spp. (MICs mostly 16-64 mg/l for Bact. fragilis and 2-8 mg/l for other bacteroides) and less active than ampicillin or cefoxitin against other anaerobes. The compound was highly resistant to hydrolysis by most beta-lactamases including OXA-1 and the enzymes from Klebsiella 1082E and Proteus vulgaris PC37 which hydrolyse cefuroxime and cefotaxime. However, it was hydrolysed slowly by the enzyme from a highly ampicillin-resistant isolate of Bact. fragilis.