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If the Albanese government wants to deliver lasting reform – in education, healthcare, housing and climate – it will have to confront the hardest political question of all: how to raise the revenue to...

Post-acute sequelae of SARS-CoV-2 (PASC) have been linked to brain alterations, but association with cognitive problems are not well understood. Here, the authors analyze blood proteins and brain MRI ...

Publications Discover our diverse collection of publications from the John Curtin Research Centre. Winning the Peace | November 2025 Safer, Stronger Sovereign | November 2025 Discussion Paper No.7 | J...

The new rules don’t address the biggest gap of all.

Contracts awarded to a company where the Australian Signals Directorate director-general’s spouse was a senior manager have been under external investigation.

The government’s deal with the Greens on environmental law reform is a political masterclass that leaves the Coalition floundering

Preventable disease is RFK, Jr's religion so I'm calling for a crusade

What on earth is going on. Seriously. Where are the doctors raising the awareness about this? Where are the journalists screaming? What is wrong with everyone? Hospital episodes for babies with heart valve problems in England. https://t.co/CCl11yI9zv

Long COVID, or postacute sequelae of COVID-19 from SARS-CoV-2 infection, is a persistent debilitating disease affecting multiple systems and organs. Long COVID pathophysiology is a complex and not fully established process. One prevailing theory is that the formation of fibrin amyloid microclots (fibrinaloids), due to SARS-CoV-2 infection, can induce persistent inflammation and capillary blockage. An association between the amyloidogenic Spike protein of SARS-CoV-2 and impaired fibrinolysis was made when it was observed that fibrin clots formed in the presence of a mixture of amyloid fibrils from the spike protein mediated resistance to plasmin lysis. Here, we use purified components from the coagulation cascade to investigate the molecular processes of impaired fibrinolysis using seven amyloidogenic SARS-COV-2 Spike peptides. Five of seven Spike amyloid fibrils appeared not to substantially interfere with the fibrinogen–fibrin–fibrinolysis process in vitro, while two spike fibrils were active in different ways. Spike601 amyloid fibrils (sequence 601–620) impaired thrombin-mediated fibrin formation by binding and sequestering fibrinogen but did not affect fibrinolysis. On the contrary, fibrin clots formed in the presence of Spike685 amyloid fibrils (sequence 685–701) exhibited a marked resistance to plasmin-mediated fibrinolysis. We conclude that Spike685 amyloid fibrils can induce dense fibrin clot networks as well as incorporate fibrin into aggregated structures that resist fibrinolysis. Our study proposes a molecular mechanism for how the Spike protein of SARS-CoV-2 could contribute to the formation of fibrinolysis-resistant microclots observed in long COVID.

A plan to capture CO2 from 13 oil sand processing facilities and store it in Alberta is threatened by cost challenges.

Opinion | 'If we give up, our collective failure will negatively impact everyone and everything'