This study presents a case for decolonising the life sciences curriculum to improve representation of the Black, Asian, and Minority Ethnic (BAME) scholars—a step in eliminating the race “awarding gap”. Here, we investigated diversity among authors in terms of ethnicity and gender of reading lists at the School of Life Sciences, University of Sussex. We show that the reading lists are not diverse and do not represent the demography of the student body. For instance, a disproportionately high number of authors in the reading lists are white 83.40 ± 5.70% (n = 977 authors), male 75.90 ± 5.40% (n = 878 authors), and of European descent. Additionally, our analysis of the geographical locations of publications reveals that a significantly high number of our materials stem from the USA or the UK, whereas the second highest global output of scientific literature (after the USA) comes from China, which is only featured in 1.02% of the reading list. Moreover, we constructively provide potential solutions to decolonise the curriculum of the University of Sussex’s School of Life Sciences by diversifying their reading lists. This study should help to establish a foundation, along with other work that is being conducted, to address the BAME awarding gap and to better showcase the work of women and ethnically underrepresented scientists in history and in modern day.

A library of thiazoles and selenothiazoles were synthesized via Ircatalyzed ylide insertion chemistry. This process is a functional group, particularly heterocycle-substituent tolerant. This was applied to the synthesis of fanetizole, an anti-inflammatory drug, and a thiazole-containing drug fragment that binds to the peptidyl-tRNA hydrolase (Pth) in Neisseria gonorrheae bacteria.

Not all treasure is silver and gold; for pathogenic bacteria, iron is the most precious and the most pillaged of metallic elements. Iron is essential for the survival and growth of all life; however free iron is scarce for bacteria inside human hosts. As a mechanism of defence, humans have evolved ways to store iron so as to render it inaccessible for invading pathogens, such as keeping the metal bound to iron-carrying proteins. For bacteria to survive within humans, they must therefore evolve counters to this defence to compete with these proteins for iron binding, or directly steal iron from them. The most populous form of iron in humans is haem: a functionally significant coordination complex that is central to oxygen transport and predominantly bound by haemoglobin. Haemoglobin is therefore the largest source of iron in humans and, as a result, bacterial pathogens in critical need of iron have evolved complex and creative ways to acquire haem from haemoglobin. Bacteria of all cell wall types have the ability to bind haemoglobin at their cell surface, to accept the haem from it and transport this to the cytoplasm for downstream uses. This review describes the systems employed by various pathogenic bacteria to utilise haemoglobin as an iron source within human hosts and discusses their contribution to virulence.