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Continued support for Uppsala Antibiotic Center in fight against antibiotic resistance

Uppsala University The Uppsala Antibiotic Center has received additional funding and is now starting 14 new doctoral projects. Five years ago, Uppsala University took a new step in the fight against accelerating antibiotic resistance with the establishment of the Uppsala Antibiotic Center. Now the centre has received a second round of funding with SEK 35 million from Uppsala University and the Swedish University of Agricultural Sciences (SLU). Fourteen new PhD projects will now begin at its research school. Antibiotics save countless lives around the world every day and have become indispensable for everything from basic medical care to advanced medicine. But what if antibiotics stop working? The development of new, globally available antibiotics is not only a public health issue but also a critical factor for our globalised society.

New model can predict how bacteria develop antibiotic resistance

New model can predict how bacteria develop antibiotic resistance

New model can predict how bacteria develop antibiotic resistance
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Study shows how new antibiotic resistance genes arise from random DNA sequences

Study shows how new antibiotic resistance genes arise from random DNA sequences An important and still unanswered question is how new genes that cause antibiotic resistance arise. In a new study, Swedish and American researchers have shown how new genes that produce resistance can arise from completely random DNA sequences. The results have been published in the journal PLOS Genetics. Antibiotic resistance is a major global problem and the spread of resistant bacteria causes disease and death, and constitutes a major cost to society. The most common way for bacteria to develop resistance is by taking up various types of resistance genes from other bacteria. These genes encode proteins (peptides) that can lead to resistance by: (i) deactivating the antibiotic, (ii) reducing its concentration, or (iii) altering the antibiotic s target so that the antibiotic can no longer bind to that target and hence halt the growth of the bacterium.

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