Diatoms are unicellular eukaryotic algae (microalgae) and one of the most common and diverse type of marine phytoplankton. Thanks to a flexible cell metabolism, they dominate in environmental conditions normally unfavorable for photosynthesis, i.e. freezing seawater, low light intensity and short photoperiod. Moreover, diatoms are able to synthesize storage lipids (20-50% of cell dry weight) that can be used for production of renewable biomass and high-value fatty acids. However, the success of these microalgae as feedstock depends on lowering the production cost. The proposed project aims to develop mixotrophic cultivation (i.e. the simultaneous use of light and carbon dioxide for photosynthesis and organic carbon for respiration) to maximize growth and outdoor productivity for selected strains from the Swedish west coast. The focus will be on the bloom-forming coastal diatom Skeletonema marinoi (S. marinoi) whose sequence annotation is ongoing, and the recent knowledge on mixotrophic growth of the model diatom Phaeodactylum tricornutum will be employed. The main objectives will be: i) using the bloom-forming S. marinoi to better understand mixotrophic metabolism in diatoms; ii) exploring the optimal mixotrophic conditions for enhanced productivity of S. marinoi; iii) investigating the potential industrial applications of S. marinoi when cultivated under mixotrophy. To achieve these objectives, an interdisciplinary approach including computational, biophysical, analytical, biotechnological and biological methods will be employed. A mixotrophic outdoor cultivation of marine microalgae in the dynamic climate of the Swedish west coast could provide a higher total production of renewable biomass for industry.

The goal of this project is to define neurological outcomes after eclampsia and to determine underlying pathophysiological pathways to eclampsia which will lead to new drugs for neuroprotection of the maternal brain. Preeclampsia and eclampsia are the most common causes of direct maternal death globally. Magnesium sulphate is the only treatment in use but it has serious side effects, only protects from seizures in 50% of cases and neuroprotection on longterm is not established. Women with eclampsia run an increased risk of longterm neurological sequelae but causality with the acute insult is not proven. There is an urgent need to understand this relationship and underlying pathophysiological pathways to identify how the acute injury affects the chronic sequelae and identify new targets for neuroprotective drugs. I want to respond to this need by determining recovery from the acute cerebral complications of eclampsia to follow up 6 months postpartum and characterize and identify pathways for neurological injury secondary to eclampsia. This will be achieved by investigating mechanisms of blood brain barrier injury, cerebral blood flow autoregulation, neuroinflammation, cognitive function deficits and white matter scarring in the brain. I will make use of a cohort of women with eclampsia from my site at Stellenbosch University, South Africa, as well as a rat model of preeclampsia and an in vitro model of preeclampsia in my lab at the University of Gothenburg, Sweden, to evaluate these outcomes. I will use anti-diabetic and anti-epileptic drugs commonly used in pregnancy and test these in rat model of preeclampsia to find new neuroprotective treatments that improve maternal outcomes. This could enable us to protect the maternal brain, save lives and reduce morbidity globally. My position as a fully trained obstetrician conducting translational research, focusing on cerebral complications makes me unique in the field and very well fitted to conduct this research project

In the healthy intestines, mucus acts as a barrier that separates the host epithelium from the microbiota and intestinal contents, as well as a habitat for commensal microbes. The major component of intestinal mucus, MUC2, is heavily O-glycosylated. Mucin O-glycans are critical for mucus barrier function and host-microbe interactions. Alterations to mucin glycosylation have been associated with diseases such as inflammatory bowel disease and cancer, and represent a novel target for therapeutic intervention. However, studies of the specific glycan structures altered during disease, as well as the consequences of these alterations on mucus barrier function and the microbiota, have been limited by a lack of tools to detect individual glycan epitopes. Mucus barrier dysfunction and microbiota dysbiosis, specifically a shift towards expansion of mucin-degrading bacteria, have been observed in response to a high fat/sugar, low fiber western-style diet (WSD). My preliminary data indicates that a WSD can also alter specific mucin glycosylation patterns. The identification of specific glycan alterations associated with a WSD creates the opportunity to study the role of individual glycan structures in mucus barrier dysfunction and microbiota composition. This study aims to 1) develop novel probes to detect specific glycan epitopes and 2) use these probes to investigate the relationships linking mucus barrier dysfunction, glycan alterations, and dysbiosis in response to a WSD. I will combine my previous experience characterizing glycan alterations in in vivo models of intestinal disease with host lab training in mucus physiology and bacterial enzyme characterization. Findings will advance our understanding of how glycosylation patterns are altered during disease, and how these alterations contribute to disease pathogenesis. This grant will allow me to enhance my skills as a researcher and give me the tools and experience necessary to establish my independent research group.

Climate change increases tree mortality worldwide, and in tropical forests in particular. While it is established that tropical tree mortality increases under hot and dry conditions, key questions regarding why and how remain unresolved. Which traits predispose trees to mortality? How does drought and heat interact to affect tropical tree growth and survival under field conditions? The overall goal of my project is to determine the sensitivity of tropical tree species to heat and drought, and based on this knowledge develop a trait-based tree mortality model that can be used to provide recommendations on which trees are suitable to different climatic regions in Rwanda, central Africa. Such recommendations are crucial for reforestation programs and climate change adaptation in Rwanda, a low-income country which has been heavily deforested in the past. To achieve this goal, I will identify which tree traits (structural, hydraulic, physiological, biochemical) that control the vitality and survival of tropical trees in multi-species plantations established at three sites in Rwanda. The sites exhibit large natural variation in precipitation and temperature, and experimental manipulations of water supply (irrigation, rainfall exclusion) are imposed at each site. Traits will be determined using a broad range of gas exchange, hydraulic and biochemical methods in the field as well as in the lab. A multi-trait model of drought- and heat-induced tree mortality will be derived based on data from the experimental sites, and evaluated using independent data from additional sites with larger trees. Based on this model, I will provide tree plantation recommendations to relevant stakeholders in Rwanda and the region. By bringing together perspectives from experimental ecology and vegetation modelling to address critical knowledge gaps this projects will make original contributions to improve the understanding and predictability of tropical tree mortality in a changing climate.