Over 10 years research and teaching experience, with significant specialised knowledge of platelet biology and transfusion science.
Can supervise: YES
My primary research interests involve investigating novel ways to manufacture or store blood components, particularly platelets. Current focus areas include:
*Platelet cryopreservation to extend the platelet shelf-life
*Platelet additive solutions to improve platelet quality
*Pathogen inactivation technology to improve platelet safety
*Introduction to Haematology and Immunology
*Med2000- Heamatology for Notre Dame post-graduate medical students
Johnson, L, Cameron, M, Waters, L, Padula, MP & Marks, DC 2019, 'The impact of refrigerated storage of UVC pathogen inactivated platelet concentrates on in vitro platelet quality parameters.', Vox sanguinis, vol. 114, no. 1, pp. 47-56.View/Download from: UTS OPUS or Publisher's site
BACKGROUND AND OBJECTIVES:Refrigeration (cold-storage) of pathogen inactivated (PI) platelet components may increase the shelf-life and safety profile of platelet components, compared to conventional room-temperature (RT) storage. Whilst there is substantial knowledge regarding the impact of these individual treatments on platelets, the combined effect has not been assessed. MATERIALS AND METHODS:Using a pool-and-split study design, paired buffy-coat derived platelets in 70% platelet additive solution (SSP+; MacoPharma) were left untreated or PI-treated using the THERAFLEX UV-Platelets System (UVC; MacoPharma). Units from each pair were split and stored at room temperature (20-24°C) or cold-stored (2-6°C) to yield RT, cold, RT-UVC and cold-UVC study groups (n = 8 in each group). In vitro quality and function was tested over 9 days. RESULTS:Cold-storage of UVC-treated platelets reduced glycolytic metabolism (glucose consumption and lactate production) compared to RT-UVC units. Cold-UVC platelets demonstrated complete abrogation of HSR by day 5, increased externalisation of phosphatidylserine (annexin-V binding) and activation of the GPIIb/IIIa receptor (PAC-1 binding) above the levels observed with the individual treatments. Aggregation responses (ADP and collagen) were enhanced in the cold-UVC platelets compared to both RT groups, but this was primarily mediated by cold-storage. Haemostatic function, as measured using TEG, was similar between the groups. CONCLUSION:Cold-storage of UVC-treated platelets reduced PI-induced acceleration of glycolytic metabolism. However, combining cold-storage and UVC-treatment resulted in additional phenotypic changes compared to each treatment individually. Further work is required to understand the impact of these changes in clinical efficacy.
Waters, L, Padula, MP, Marks, DC & Johnson, L 2019, 'Cryopreservation of UVC pathogen-inactivated platelets.', Transfusion, vol. 59, no. 6, pp. 2093-2102.View/Download from: UTS OPUS or Publisher's site
BACKGROUND:Extending the platelet (PLT) shelf life and enhancing product safety may be achieved by combining cryopreservation and pathogen inactivation (PI). Although studied individually, limited investigations into combining these treatments has been performed. The aim of this study was to investigate the effect of PI treating PLTs before cryopreservation on in vitro PLT quality and function. STUDY DESIGN AND METHODS:ABO-matched buffy coat-derived PLTs in PLT additive solution (SSP+; Macopharma) were pooled and split to form matched pairs (n = 8). One unit remained untreated and the other was treated with the THERAFLEX UV-Platelets System (UVC; Macopharma). For cryopreservation, 5% to 6% dimethyl sulfoxide was added to the PLTs, and they were frozen at -80°C. After being thawed, untreated cryopreserved PLTs (CPPs) and UVC-treated CPPs (UVC-CPPs) were resuspended in plasma. In vitro quality was assessed immediately after thawing and after 24 hours of room temperature storage. RESULTS:UVC-CPPs had lower in vitro recovery compared to CPPs. By flow cytometry, PLTs demonstrated a similar abundance of GPIX (CD42a), GPIIb (CD41a), and GPIbα (CD42b-HIP1), while the activation of GPIIb/IIIa (PAC-1) was increased in UVC-CPPs compared to CPPs. UVC-CPPs demonstrated greater phosphatidylserine exposure (annexin V) and microparticle shedding but similar P-selectin (CD62P) abundance compared to CPPs. UVC-CPPs displayed similar functionality to CPPs when assessed using aggregometry, thromboelastography, and thrombin generation. CONCLUSIONS:This study demonstrates the feasibility of cryopreserving UVC-PI-treated PLT products. UVC-PI treatment may increase the susceptibility of PLTs to damage caused during cryopreservation, but this is more pronounced during postthaw storage at room temperature.
Johnson, L, Tan, S, Jenkins, E, Wood, B & Marks, DC 2018, 'Characterization of biologic response modifiers in the supernatant of conventional, refrigerated, and cryopreserved platelets', TRANSFUSION, vol. 58, no. 4, pp. 927-937.View/Download from: UTS OPUS or Publisher's site
Reid, S, Johnson, LN, Woodland, NB & Marks, D 2012, 'Pathogen reduction treatment of buffy coat platelet concentrates in additive solution induces proapoptotic signaling', Transfusion, vol. 52, no. 10, pp. 2094-2103.View/Download from: UTS OPUS or Publisher's site
BACKGROUND: Pathogen reduction technology (PRT) can potentially reduce the risk of transfusion-transmitted infections. However, PRT treatment of platelet (PLT) concentrates also results in reduced PLT quality and increased markers of apoptosis during storage. The aim of this study was to investigate changes to the expression and activation of proteins involved in apoptosis signaling. STUDY DESIGN AND METHODS: Samples from riboflavin and ultraviolet light PRT-treated and untreated (control) buffy coatderived PCs in 70% SSP+ and 30% plasma were taken on Days 1, 5, and 7 of storage. Phosphatidylserine (PS) exposure, expression of Bcl-2 family proteins, cytochrome c release, and cleavage of caspase-3 and caspase-3 substrates were analyzed using flow cytometry and Western blotting. RESULTS: Compared to untreated controls, markers of apoptosis signaling were increased after PRT and subsequent storage. PS exposure on the PLT outer membrane was significantly higher after PRT on Days 5 and 7 of storage (p < 0.05). Expression of proapoptotic Bak and Bax was higher after PRT and subsequent storage. Cytochrome c release and caspase-3 cleavage were also greater and occurred earlier in the PRT-treated PLTs. The cleavage of caspase-3 substrates gelsolin and ROCK I were also increased after PRT, compared to untreated controls. CONCLUSIONS: This study demonstrated an increase in proapoptotic signaling during PLT storage, which was exacerbated by PRT. Many of these differences emerged outside the current 5-day storage period. These changes may not currently influence PLT transfusion quality, but will need to be carefully evaluated when considering extending PLT storage beyond 5 days
Australian Red Cross Blood Service