Diagnostic digital pathology implementation: learning from the digital health experience

Digital Pathology (also referred to as Telepathology and Whole Slide Imaging) is the process of producing high resolution digital images from tissue sections on glass slides. These glass slides are normally examined under a microscope by a pathologist as part of the diagnostic process. The emergence of digital pathology now means that digital images are stored on secure servers and can be viewed on computer monitors; enabling pathologists to work remotely and to collaborate with other colleagues when second opinions are needed. The implementation of digital pathology into clinical practice has many potential benefits. Although this has been long recognised, its adoption as a diagnostic tool remains low and pathologists’ projections about its future deployment are cautious. Notable early digital pathology adopters have led the way. The challenge now is to scale-up digital pathology beyond the relatively few large networks and centres of excellence. Many other areas of healthcare have accumulated experience about optimising approaches to digital health/healthcare technology deployment and sustainability. This has been done in a multi-disciplinary context and has applied theoretical/conceptual frameworks. Thus far there has been little use of similar frameworks in the planning of digital pathology deployment in clinical practice. In this essay, I will explore the scope of digital pathology implementation approaches that have been deployed in clinical practice and examine what can be learned from the wider healthcare experience of adopting, scaling-up and sustaining innovative healthcare solutions

Calcineurin Inhibition at the Clinical Phase of Prion Disease Reduces Neurodegeneration, Improves Behavioral Alterations and Increases Animal Survival

Prion diseases are fatal neurodegenerative disorders characterized by a long pre-symptomatic phase followed by rapid and progressive clinical phase. Although rare in humans, the unconventional infectious nature of the disease raises the potential for an epidemic. Unfortunately, no treatment is currently available. The hallmark event in prion diseases is the accumulation of a misfolded and infectious form of the prion protein (PrPSc). Previous reports have shown that PrPSc induces endoplasmic reticulum stress and changes in calcium homeostasis in the brain of affected individuals. In this study we show that the calcium-dependent phosphatase Calcineurin (CaN) is hyperactivated both in vitro and in vivo as a result of PrPSc formation. CaN activation mediates prion-induced neurodegeneration, suggesting that inhibition of this phosphatase could be a target for therapy. To test this hypothesis, prion infected wild type mice were treated intra-peritoneally with the CaN inhibitor FK506 at the clinical phase of the disease. Treated animals exhibited reduced severity of the clinical abnormalities and increased survival time compared to vehicle treated controls. Treatment also led to a significant increase in the brain levels of the CaN downstream targets pCREB and pBAD, which paralleled the decrease of CaN activity. Importantly, we observed a lower degree of neurodegeneration in animals treated with the drug as revealed by a higher number of neurons and a lower quantity of degenerating nerve cells. These changes were not dependent on PrPSc formation, since the protein accumulated in the brain to the same levels as in the untreated mice. Our findings contribute to an understanding of the mechanism of neurodegeneration in prion diseases and more importantly may provide a novel strategy for therapy that is beneficial at the clinical phase of the disease

Inflammatory response in a mouse model of scrapie

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