It is now well established that atherosclerosis is an inflammatory disease with a broad array of inflammatory cells and pathways implicated at every stage of the disease . Acute and chronic inflammation are key factors in the development of endothelial damage [2,3]. As endothelial dysfunction is a validated biomarker for future cardiovascular events, closer study of the role of inflammation in early-stage endothelial dysfunction should be undertaken, particularly in high risk populations.
Background: Cyclin subunits, in combination with their Cyclin-dependent kinase (Cdk) domains, regulate many aspects of cell cycle progression, including DNA replication (Cyclin A2) and cell division (Cyclin B1). Cyclin A2 and Cyclin B1 share the same catalytic subunits, Cdk1 and Cdk2, therefore it is difficult to separate their functions because Cdk1 or Cdk2 inhibitors affect multiple Cyclin/Cdk complexes at once. For example, Cyclin B/Cdk1 is known to stimulate mitotic entry but Cyclin A2/Cdk1 could well play an important undiscovered role.
Wnt signalling was first discovered in tumour models and has been recognized as a key regulator in cancer for several decades. This has prompted a number of researchers and pharmaceutical companies to develop Wnt-modulating drugs for cancer treatment. However, we are still learning about the complex and often context-dependent effects of WNT signalling in differing tumour types, so it is important to understand the role of Wnt signalling in individual cancers before Wnt-modulating therapeutics can be used to treat patients.
Tumour heterogeneity, as measured in various imaging modalities including MRI, has been reported to useful in prognostication and in the identification of patients who will achieve a complete response to neoadjuvant chemotherapy (NAC). Heterogeneity considers microscopic image ‘texture’, by mapping and modelling grey-level distributions of individual pixels within regions of interest; textural analysis (TA). It has been hypothesised that TA indirectly links to lesion pathology via tissue structure, which influences the contrast in the final MR image.
The DNA Damage Response (DDR) is a major component of a cells defence against disease. It serves to recognize and repair DNA damage, regulate gene expression, control cell-cycle progression and where necessary, to promote programmed cell death.
Adverse early life experiences, in the form of poor maternal care, are recognized to program an abnormal stress response, which increases the risk of psychiatric disorders e.g. depression in adulthood. Moreover, the impact of adverse early-life experiences has the potential to extend to future generations, suggesting a contribution by genetic and possibly, epigenetic factors. The mechanisms of stress dysfunction are complex, but may involve inhibitory GABAA receptors (GABAARs), as these receptors crucially curtail stress-induced activation of the HPA axis.