Environmental Sustainability in the Cardiac Catheter Laboratory.

The health care sector contributes to nearly 5% of global carbon emissions with the exponential growth of medical waste posing a significant challenge to environmental sustainability. As the impact of climate change on individuals and population health becomes increasingly more apparent, the health care system's significant impact on the environment is also raising concerns. Hospitals contribute disproportionately to health care waste with the majority arising from resource intensive areas such as operating theatres and cardiac catheter labs (CCLs). Despite the growing volume of cardiac procedures worldwide, initiatives to reduce waste from CCLs have received limited attention, overlooking opportunities for significant reduction in operational costs and carbon footprint. We aim to raise awareness of the current landscape of waste management in CCLs. We identify areas of resource optimisation and highlight practical strategies and frameworks employed elsewhere in health care to reduce waste. Importantly, we hope to empower health care workers in CCLs to make a meaningful change to their practice and contribute towards a more sustainable future.

ß2GPI exerts an anti-obesity effect in female mice by inhibiting lipogenesis and promoting lipolysis.

In humans, males compared to females have increased visceral adipose tissue which contributes to their increased risk of early death. Mice display analogous sexual diamorphism whereby females are protected from weight gain when fed a high fat diet compared to males. A role has recently been reported for ß2-glycoprotein I, an abundant plasma protein, in healthy leanness in humans. In this study we investigated the role of ß2-glycoprotein I in fat metabolism in male and female mice fed a normal chow or high fat diet. We have made a number of novel insights into factors contributing to sexual diamorphism in obesity. Female wild type mice are protected from obesity when fed a high fat diet due to down regulation of lipogenesis in the visceral adipose tissues. This down regulation is due to ß2-glycoprotein I as female mice deficient in this protein have increased levels of lipogenesis enzymes in their visceral adipose tissues with an accompanying increase in weight compared to female wild type controls. Understanding female specific regulators of obesity may lead to sex specific anti-obesity therapies to address this major health problem.

Βeta 2-glycoprotein I protects mice against gram-negative septicaemia in a sexually dimorphic manner.

The immune responses of males and females to bacterial infections display differences. The mechanisms that underlie this sexual dimorphism are multifactorial. Lipopolysaccharide (LPS) contributes to the pathogenesis of endotoxaemia. We have previously demonstrated that the plasma protein beta-2 glycoprotein-1 (ß2GPI) reduces LPS-induced inflammation in male mice. In the present study using a more robust infection model of septicaemia the role of ß2GPI is examined in both male and female wild type (WT) and ß2GPI deficient (ß2GPI-/-) mice challenged with Escherichia coli (E. coli) intravenously. ß2GPI deficiency led to an increase of E. coli colony forming units (CFU) in the circulation of both male and female mice. In male ß2GPI-/- mice this was associated with a worse clinical severity score. This difference was not observed between female ß2GPI-/- and female WT mice. Male WT mice had decreased levels of total and increased levels of free thiol ß2GPI following administration of LPS or E. coli. This pattern of sexual dimorphic response was also observed in our cohort of humans with sepsis. These findings support a role for ß2GPI in modulating the sex-specific susceptibility to gram-negative septicaemia.