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Transformants exhibited lower carbapenem MICs than did clinical isolates, likely reflecting total β-lactamase content and additional resistance mechanisms such as porin mutations in the clinical isolates (Table 2).
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BALB/c mice inoculated with transformants exhibited higher weights, lower histological lesions and lower M. tuberculosis inoculum in the liver, spleen and lungs than control mice challenged with wild-type M. tuberculosis.
JFH1/5AC-Q24K/L28M/R30Q/A92K exhibited lower replication and virus production efficiencies.
The pattern VEP exhibited lower amplitudes and prolonged peak times.
The injured paw exhibited lower reaction latency.
However, the transformants exhibited no improved tolerance against desiccation stress.
Resultant transformants exhibited salt-tolerance with dwarfing phenotypes.
The transformants exhibited higher tolerance to NaCl stress compared to untransformed parent plants.
All the uidA transformants had the "yellow-in-the-dark" phenotype characteristic of chlL mutants, whereas homoplasmic nifH transformants exhibited a partial "green-in-the-dark" phenotype.
Compared to the wild type, the PYC activity in the pyc transformants increased 56%83%%, whereas pepc transformants exhibited significant PEPC activity (3 6 mU/mg) that was absent in the wild type.
The I-SceI enzyme mediated integration, or SEMI, in combination with a Δtku70 mutant has a synergistic effect on homologous recombination efficiencies as 90 100% of the transformants exhibited integration of the expression cassette at the homologous site.
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