ArticleBMC medicine2015
Observing in real time the evolution of artemisinin resistance in Plasmodium falciparum.
Article in BMC medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Discovery of isoxazolyl-based inhibitors ofRSC medicinal chemistry · 2020Article
- Development of Chemical Entities Endowed with Potent Fast-Killing Properties againstJournal of medicinal chemistry · 2019Article
- Resistance screening and trend analysis of imported falciparum malaria in NSW, Australia (2010 to 2016).PloS one · 2018Article
- A potent series targeting the malarial cGMP-dependent protein kinase clears infection and blocks transmission.Nature communications · 2017Article
- K13-Propeller Polymorphisms in Plasmodium falciparum Isolates from Patients in Mayotte in 2013 and 2014.Antimicrobial agents and chemotherapy · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Simple genetic changes that correlate with drug resistance are used routinely to identify resistant pathogens. These "molecular markers" have usually been defined long after the phenotype of resistance was noted. The molecular changes at the "end game" reflect a long and complex evolution of genetic changes, but once a solidly resistant set of changes assembles under drug selection, that genotype is likely to become fixed, and resistant pathogens will spread widely. Artemisinins are currently used worldwide to treat malaria caused by Plasmodium falciparum, but parasite response has diminished rapidly in the Mekong region of Southeast Asia. Should artemisinins lose potency completely and this effect spread worldwide, effective malaria treatment would be almost impossible. The full range of modern methods has been applied to define rapidly the genetic changes responsible. Changes associated with artemisinin resistance are complex and seem to be evolving rapidly, especially in Southeast Asia. This is a rare chance to observe the early stages in evolution of resistance, and to develop strategies to reverse or mitigate the trend and to protect these key medicines.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.