Climate-influenced vector-borne diseases in Africa: a call to empower the next generation of African researchers for sustainable solutions.

We look at the link between climate change and vector-borne diseases in low- and middle-income countries in Africa. The large endemicity and escalating threat of diseases such as malaria and arboviral diseases, intensified by climate change, disproportionately affects vulnerable communities globally. We highlight the urgency of prioritizing research and development, advocating for robust scientific inquiry to promote adaptation strategies, and the vital role that the next generation of African research leaders will play in addressing these challenges. Despite significant challenges such as funding shortages within countries, various pan-African-oriented funding bodies such as the African Academy of Sciences, the Africa Research Excellence Fund, the Wellcome Trust, the U.S. National Institutes of Health, and the Bill and Melinda Gates Foundation as well as initiatives such as the African Research Initiative for Scientific Excellence and the Pan-African Mosquito Control Association, have empowered (or are empowering) these researchers by supporting capacity building activities, including continental and global networking, skill development, mentoring, and African-led research. This article underscores the urgency of increased national investment in research, proposing the establishment of research government agencies to drive evidence-based interventions. Collaboration between governments and scientific communities, sustained by pan-African funding bodies, is crucial. Through these efforts, African nations are likely to enhance the resilience and adaptive capacity of their systems and communities by navigating these challenges effectively, fostering scientific excellence and implementing transformative solutions against climate-sensitive vector-borne diseases.

What supervisors and universities can do to enhance doctoral student experience (and how they can help themselves).

Over the past two decades, there has been a flurry of government papers and policy reports worldwide calling for increased number and diversity of doctoral researchers and a broadening of the curriculum to meet the developing needs of respective national 'knowledge-driven' economies. This has been followed by position papers and best practice examples of employability skills development in boundary-crossing doctoral programmes, especially in response to these initiatives. However, there is a disassociation between this ample literature expounding the new doctorate with its broader remit, inclusivity and production of 'industry-ready' graduates and the comparatively sparse literature on the doctoral candidates' experiences of their programmes and career readiness. Within this review, we briefly outline international government initiatives and examples of the responses by Life Science and Biomedical doctoral programmes to address these various challenges. Furthermore, we explore the recent literature on the lived experience of doctoral researchers by examining their perception of the recent changes to the research context to make recommendations for universities and supervisors on how to better support an ever more diverse doctoral population for a wide range of career opportunities. Examples of how doctoral researchers themselves can make the best of currently available opportunities are also provided.

Decreased firing of striatal neurons related to licking during acquisition and overtraining of a licking task.

Neurons that fire in relation to licking, in the ventral part of the dorsolateral striatum (DLS), were studied during acquisition and performance of a licking task in rats for 14 sessions (2 h/d). Task learning was indicated by fewer errors of omission of licking and improved movement efficiency (i.e., shorter lick duration) over sessions. Number of licks did not change over sessions. Overtraining did not result in habit formation, as indicated by similar reductions of licking responses following devaluation by satiety in both early and late sessions. Twenty-nine lick neurons recorded and tracked over sessions exhibited a significant linear decrease in average firing rate across all neurons over sessions, correlating with concurrent declines in lick duration. Individually, most neurons (86%) exhibited decreased firing rates, while a small proportion (14%) exhibited increased firing rates, during lick movements that were matched over sessions. Reward manipulations did not alter firing patterns over sessions. Aside from the absence of habit formation, striatal processing during unconditioned movements (i.e., licking) was characterized by high activity of movement-related neurons during early performance and decreased activity of the same neurons during overtraining, similar to our previous report of head movement neurons during acquired, skilled, instrumental head movements that ultimately became habitual (Tang et al., 2007). Decreased activity in DLS neurons may reflect a common neural mechanism underlying improvement in movement efficiency with overtraining. Nonetheless, the decreased striatal firing in relation to a movement that did not become habitual demonstrates that not all DLS changes reflect habit formation.

Dose- and rate-dependent effects of cocaine on striatal firing related to licking.

To examine the role of striatal mechanisms in cocaine-induced stereotyped licking, we investigated the acute effects of cocaine on striatal neurons in awake, freely moving rats before and after cocaine administration (0, 5, 10, or 20 mg/kg). Stereotyped licking was induced only by the high dose. Relative to control (saline), cocaine reduced lick duration and concurrently increased interlick interval, particularly at the high dose, but it did not affect licking rhythm. Firing rates of striatal neurons phasically related to licking movements were compared between matched licks before and after injection, minimizing any influence of sensorimotor variables on changes in firing. Both increases and decreases in average firing rate of striatal neurons were observed after cocaine injection, and these changes exhibited a dose-dependent pattern that strongly depended on predrug firing rate. At the middle and high doses relative to the saline group, the average firing rates of slow firing neurons were increased by cocaine, resulting from a general elevation of movement-related firing rates. In contrast, fast firing neurons showed decreased average firing rates only in the high-dose group, with reduced firing rates across the entire range for these neurons. Our findings suggest that at the high dose, increased phasic activity of slow firing striatal neurons and simultaneously reduced phasic activity of fast firing striatal neurons may contribute, respectively, to the continual initiation of stereotypic movements and the absence of longer movements.

The microglial gene regulatory network activated by interferon-gamma.

We have analysed the microglial pathway stimulated by interferon-gamma (IFN-gamma) using an in silico approach employing a database of eukaryotic molecular interactions and a microarray dataset validated by quantitative real-time PCR (qRT-PCR). Following IFN-gamma stimulation, production of neuroprotective factors by microglia was found to be reduced while caspase 1 and serping1 which are involved in cell death cascades are up-regulated suggesting a safeguarding mechanism. Extracellular matrix interactions and intracellular protein degradation are altered in concert with these changes. The regulatory network of IFN-gamma responsive microglial genes is outlined in detail and differentially expressed genes are mapped to their respective cellular compartments. A pathway approach to the analysis of microarray data is advocated since overlaying pathway and actual expression data as shown here greatly facilitates understanding the biological meaning of a gene regulatory network. In addition, genes of similar function that are differentially regulated are less likely to be false positives than single unrelated genes.