scispace - formally typeset
D

Diana Machado

Researcher at Universidade Nova de Lisboa

Publications -  75
Citations -  2535

Diana Machado is an academic researcher from Universidade Nova de Lisboa. The author has contributed to research in topics: Mycobacterium tuberculosis & Efflux. The author has an hindex of 25, co-authored 71 publications receiving 1935 citations. Previous affiliations of Diana Machado include University of Lisbon.

Papers
More filters
Journal ArticleDOI

Mode of action of the 2-phenylquinoline efflux inhibitor PQQ4R against Escherichia coli

TL;DR: In this article, the authors described the mode of action of the 2-phenylquinoline efflux inhibitor (4-(piperazin-1-yl)ethoxy)-2-(4-propoxyphenyl) quinolone -PQQ4R against Escherichia coli, by studding its efflux inhibitory ability, its synergistic activity in combination with antibiotics, and compared its effects with the inhibitors phenyl-arginine-β-naphthylamide (PAβN) and chlorpromazine (CPZ).
Journal ArticleDOI

Contribution of efflux to colistin heteroresistance in a multidrug resistant Acinetobacter baumannii clinical isolate.

TL;DR: In this paper, the role of efflux in colistin-heteroresistant populations of Acinetobacter baumannii clinical isolate was investigated by synergistic assays with efflux inhibitors, real-time efflux activity measurements and analysis of the mRNA transcriptional levels of selected efflux pump genes.
Journal ArticleDOI

Design, synthesis, and evaluation of new 2-(quinoline-4-yloxy)acetamide-based antituberculosis agents.

TL;DR: Using a classical molecular simplification approach, a series of 36 quinolines were synthesized and evaluated as in Vitro inhibitors of Mycobacterium tuberculosis growth, indicating that this class of compounds may furnish candidates for the future development of antituberculosis drugs.
Journal ArticleDOI

From multidrug-resistant to extensively drug-resistant tuberculosis in Lisbon, Portugal: the stepwise mode of resistance acquisition

TL;DR: Analysis of the distribution of the mutations found by genetic clustering showed that in the Q1 cluster, two mutations were enough to ensure development of XDR-TB from an MDR strain, revealing that eis G-10A mutations may result in amikacin resistance undetectable by widely used phenotypic assays.