Andy
Retired committee member
From their home page - https://www.melbournebioanalytics.org/
From their Projects page - https://www.melbournebioanalytics.org/projects/
This is the home of Melbourne Bioanalytics, an Australian research group specialising in metabolomics, genomics and microbiomics research into Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).
ME/CFS is a severe, chronic and disabling multisystem disease which affects an estimated 240,000 Australians, and as many as 17 million people worldwide. For many the condition will be lifelong, limiting their ability to work, study or even leave their beds. There is currently no diagnostic test, nor cure for the disease.
ME/CFS research is underfunded globally. Research funding for similarly disabling conditions is 25 times higher than funding for ME/CFS research. In Australia, biomedical research into ME/CFS has received no federal government funding since 2005.
Make a donation to help Melbourne Bioanalytics continue their ground-breaking work into ME/CFS.
This website is run by patients, to promote and raise much needed funds for the research work of Melbourne Bioanalytics.
From their Projects page - https://www.melbournebioanalytics.org/projects/
Longitudinal Study
Longitudinal Metabolic and Genomic Study
Aim: Monitor how metabolic pathways change in ME/CFS patients over a short-term stress event and over the long-term maintenance of the disorder.
All previous metabolomics research on ME/CFS has viewed the metabolites in a single urine, blood and fecal sample from a cohort of patients with ME/CFS and non-ME/CFS controls, many significant differences were observed between the two groups and we have highlighted biological pathways that we hypothesise to be significant to the disorder. We previously have observed energy metabolism and oxidative stress issues are apparent in ME/CFS and that the energy metabolism in particularare associated with gut microbiota and metabolite changes. The next step is to determine how these pathways interact and whether they are causal or symptomatic of ME/CFS. To do this we plan to look at the metabolite changes over multiple sampling points in time from each individual while also viewing the genes that are being expressed over those sample points.
B Cell Maturation
Metabolic Analysis of B Cell Maturation
Collaboration project with Fane Mensah and Professor Jo Cambridge at University College London
Aim: Monitor the metabolic requirements of B cell maturation to observe if altered metabolic environments impact B cell maturation and, conversely, if B cell maturation alters the metabolic environment.
Previous research has found consistent evidence of abnormalities in the immune system, energy metabolism and oxidative stress in ME/CFS patients. Promising improvement after B-cell depletion therapy with Rituximab highlighted the possible involvement of the immune system and (in this case B cells) in ME/CFS.
Fane Mensah and Jo Cambridge have found abnormalities in the maturation of B cells, observing phenotypic markers on B cell subsets and anomalies of mitochondrial mass. We now want to find out the metabolic requirements for B cells and to see if there are differences between the metabolism of ME/CFS and non-ME/CFS B cells. We also want to know if the B cells impact the metabolic environment and conversely if the metabolic environment impacts the B cells.
To read more on each project click through to the project page, https://www.melbournebioanalytics.org/projects/, and then click on the appropriate option.Mitochondria
Mitochondrial Respiratory Function and Cellular Metabolism in Lymphoblasts
Collaboration project with Daniel Missailidis and Professor Paul Fisher at LaTrobe University
Aim: Evaluate mitochondrial and cellular energy pathways to resolve the foundation of the energy anomalies that have been observed from metabolic studies on ME/CFS patients.
Mitochondria are structures present within the cells of our body and most prominently produce ATP via aerobic respiration – this is akey component of cellular energy supply. Mitochondrial energy production relies upon oxygen and has several key pathways that lead to energy production. We can measure oxygen consumption by cells in real time, which enables the input of enzyme inhibitors of mitochondrial processes to be added. The end-product of such an assay is to see the maximum energy production from mitochondria as it loses important pathways step-by-step. This allows us to pinpoint the areas in the mitochondria that differ between ME/CFS and non-ME/CFS groups