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How do I know who my advisor is? Can I change my advisor?

​For M.S. students, your advisor when you are admitted to KAUST is the Program Chair. For Ph.D. students, your advisor is your PI (supervisor) whose lab you have been accepted in to. 

Yes, you can change your advisor. M.S. students are advised to do so if/when they begin their thesis or directed research.  Ph.D. students do have the ability to change advisors, but the overall impact to the Ph.D. project, as well as the time left to finish the Ph.D., could be significant.  This will have to be taken into account before approval.

​M.S. students need 36 credits (combination of courses and research is specific to your program). 

Ph.D. students need 6 credits of 300-level coursework and will earn dissertation research credit each semester until they defend (no minimum credits established, although there is a minimum residency requirement of 2.5 years).

​During your final M.S. semester at KAUST, you will be eligible to submit a “rollover” application.  You will be contacted by the Admissions Office for this.  You must have a confirmed supervisor in order for the application to be approved.

​M.S. students get all university holidays (Eid Al-Fitr, Eid Al-Adha, Spring break).  

Ph.D. students get university holidays and three weeks of annual/vacation leave per calendar year to be taken in agreement with your PI.

​Mandatory, core and elective courses are listed in the program guide. The program guides for all BESE programs can be found here 
​“Time Extension to Complete M.S. Thesis” application request can be submitted by the 9th week of your final Fall semester.  See application for required approvals here .
​No.  Only once during your time here at KAUST.  If “WE Courses” appears on your KAUST transcript, that means you have met this requirement.​
​Yes, both M.S. and Ph.D. in all BESE programs must register, attend, and receive an S grade for the graduate seminar each semester (Spring and Fall, NOT summer).

​Yes. Drop and Add deadlines are on the academic calendar.

​Your GPC can help you request these from the Registrar’s Office, or you can contact them directly at  RegistrarHelpDesk@KAUST.EDU.SA​​ 

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Transcriptional impact of cytoadherence and stimulation on microvascular endothelium

Abstract:
Cerebral malaria (CM) is the most prevalent and deadly complication of severe Plasmodium falciparum infection. A hallmark of CM is the sequestration of Plasmodium falciparum-infected erythrocytes (IE) within the brain microvasculature. The binding of IE to endothelium reduces microvascular flow and combined with an inflammatory response, perturbs endothelial barrier function, resulting in the breakdown of the blood-brain barrier. Cytoadherence leads to activation of the endothelium and alters a range of cell processes affecting signalling pathways, receptor expression, coagulation, and disruption of BBB integrity. This binding to the endothelium is mediated by Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1), which is expressed on IE and composed of different adhesion domains that may characterise host-receptor binding. In conjunction with IE sequestration, inflammation leads to the production of the pro-inflammatory cytokine tumour necrosis factor (TNF), which in turn activates the endothelium. To that end, we investigated whether CM-derived parasites elicit differential effects on human brain microvascular endothelial cells (HBMECs), as compared to uncomplicated malaria (UM) derived parasites using probe-based gene expression assays. We observed a significant effect on the endothelial transcriptional response in the presence of IE, yet there is no significant correlation between HBMEC responses and the type of clinical syndrome (UM or CM). Further, there was no correlation between HBMEC gene expression and both binding itself and the level of IE binding to HBMEC. Following on from this, the patient-derived isolates were sequenced to explore the diversity of the predicted PfEMP1 adhesion domains. Additionally, bulk RNA-sequencing was utilised to examine the transcriptional profiles of two types of microvascular endothelial cells stimulated with varied concentrations of TNF over a short time course in vitro. It was observed that temporal modulation had a greater impact on differential gene expression when compared to the differences between the two dosing treatments. Despite being distinct cell types, these microvascular endothelial cells shared a proportion of shared upregulated differentially expressed genes. Overall, this study provides further insight into the dynamic effects of patient-derived parasite isolates and TNF on the transcriptional responses of microvascular endothelium.

Bio:
Caroline Askonas is a PhD candidate in Bioscience in the Pathogen Genomics Laboratory under the supervision of Professor Arnab Pain. Her work focuses on host-pathogen interactions in malaria. Caroline obtained her BSc in Chemistry from Hope College in the USA followed by an MSc in Immunology of Infectious Diseases from the London School of Hygiene and Tropical Medicine in the UK.

Speakers

Caroline Askonas

​LIFE AT KAUST