Nhi Hin - PhD Candidate
The molecular signature of Alzheimer's disease
Principle supervisor Associate Professor Michael Lardelli, School of Biological Sciences
Ning Liu - PhD Candidate
Investigating Three Dimensional Chromosome Structure in T Lymphocytes using High-Resolution Chromosome Conformation Capture Assays
Weixiong He - Master of Biotechnology
Creating computational workflows and pipelines for methylation quantitative trait loci (meQTL) analyses in human placental data
Guanchen Li - Master of Biotechnology
Using SNP calling methods and Next-Generation Sequencing for identification of degraded human remains
Tianzhi Yu – Master of Biotechnology
RNA-Seq time course of mouse endometriosis model
Principal supervisor Steve Pederson, Bioinformatics Hub Co-supervisor Dr John Schjenken, Robinson Research Institute
Endometriosis is a gynaecological disease characterized by the growth of estrogen-responsive endometrial tissue (normally lined inside of the uterus) outside the uterine cavity. i.e. Endometriosis is characterized by endometrial tissue being ‘in the wrong place’. This disease affecting ~10% of reproductive-aged women worldwide. Despite its prevalence, the pathogenesis of endometriosis remains unclear. Most people believe that endometriosis is caused by the reflux of menstrual blood (containing endometrial fragments) into peritoneal cavity (having 85% of macrophages).
The presence of endometrial fragments leads to the recruitment of inflammatory cells, especially, a large number of macrophages. As macrophages arrive at the site, they can be then activated towards M1 subclass (classic activation) by exposing to inflammation-related cytokines. Studies demonstrated that M1 macrophages are highly specialized in removal of debris. So large amount of shed endometrial cells are cleaned and the level of pro-inflammatory cytokines are therefore reduced (i.e. the resolution of inflammatory). So, the recruited macrophages cannot become M1 in time; they don’t work properly to engulf the shed endometrial cells, and therefore, these endometrial cells will get a chance to stick to the surfaces/organs in the cavity. As the anti-inflammatory molecules increased, macrophages are polarized towards M2 subtype (alternative activation), helping the attached endometrial tissue to repair, proliferate, and eventually establish the lesions.
Previous studies have shown that miRNA-155 promotes M1 macrophage activation whereas miRNA-223 is involved in M2 macrophage polarization. Therefore, Robinson Research Institute developed miR-223-deficient and miR-155-deficient homologous mice models, in order to study the functional alteration of macrophages and the development of endometriotic lesions. The objective of my study is, to analyse the differential expression of mRNA in these miRNA-deficient mice models with the endometriotic-like disease and compare this mRNA expression profile to that in humans, by using mRNA-seq. In order to predict the pathways and gens associated with lesion development.
Jacqueline Rehn - Master of Biotechnology
The role of DNA damage in ancient metagenomic studies
Kelly Ren - Master of Biotechnology
DNA-methylated differences in monozygotic twins discordant for unipolar and bipolar depression
Awais Choudhry - B.Sc (Honours)
Aristaless related X-linked Intellectual Disability