From Scope to Screen: The Evolution of Histology Education.

Histology, the branch of anatomy also known as microscopic anatomy, is the study of the structure and function of the body's tissues. To gain an understanding of the tissues of the body is to learn the foundational underpinnings of anatomy and achieve a deeper, more intimate insight into how the body is constructed, functions, and undergoes pathological change. Histology, therefore, is an integral element of basic science education within today's medical curricula. Its development as a discipline is inextricably linked to the evolution of the technology that allows us to visualize it. This chapter takes us on the journey through the past, present, and future of histology and its education; from technologies grounded in ancient understanding and control of the properties of light, to the ingenuity of crafting glass lenses that led to the construction of the first microscopes; traversing the second revolution in histology through the development of modern histological techniques and methods of digital and virtual microscopy, which allows learners to visualize histology anywhere, at any time; to the future of histology that allows flexible self-directed learning through social media, live-streaming, and virtual reality as a result of the powerful smart technologies we all carry around in our pockets. But, is our continuous pursuit of technological advancement projecting us towards a dystopian world where machines with artificial intelligence learn how to read histological slides and diagnose the diseases in the very humans that built them?

Non-muscle myosins 2A and 2B drive changes in cell morphology that occur as myoblasts align and fuse.

The interaction of non-muscle myosins 2A and 2B with actin may drive changes in cell movement, shape and adhesion. To investigate this, we used cultured myoblasts as a model system. These cells characteristically change shape from triangular to bipolar when they form groups of aligned cells. Antisense oligonucleotide knockdown of non-muscle myosin 2A, but not non-muscle myosin 2B, inhibited this shape change, interfered with cell-cell adhesion, had a minor effect on tail retraction and prevented myoblast fusion. By contrast, non-muscle myosin 2B knockdown markedly inhibited tail retraction, increasing cell length by over 200% by 72 hours compared with controls. In addition it interfered with nuclei redistribution in myotubes. Non-muscle myosin 2C is not involved as western analysis showed that it is not expressed in myoblasts, but only in myotubes. To understand why non-muscle myosins 2A and 2B have such different roles, we analysed their distributions by immuno-electron microscopy, and found that non-muscle myosin 2A was more tightly associated with the plasma membrane than non-muscle myosin 2B. This suggests that non-muscle myosin 2A is more important for bipolar shape formation and adhesion owing to its preferential interaction with membrane-associated actin, whereas the role of non-muscle myosin 2B in retraction prevents over-elongation of myoblasts.

Actin filament organization in aligned prefusion myoblasts.

The organization of the actin cytoskeleton in prefusion aligning myoblasts is likely to be important for their shape and interaction. We investigated actin filament organization and polarity by transmission electron microscopy (TEM) in these cells. About 84% of the filaments counted were either found in a subplasmalemma sheet up to 0.5 microm thick that was aligned with the long axis of the cell, or in protrusions. The remaining filaments were found in the cytoplasm, where they were randomly orientated and not organized into bundles. The polarity of the subplasmalemma filaments changed progressively from one end of the cell to the other. At the ends of the cells and in protrusions, the majority of filaments were organized such that their barbed ends faced the tip of the protrusion. We did not find any actin filament bundles or stress fibres in these cells. Time-lapse phase microscopy demonstrated that aligned cells were still actively migrating at the time of our TEM observations, and their direction of movement was restricted to the long axis of the cell group. The ability of these cells to locomote actively in the absence of actin filament bundles suggests that in these cells the subplasmalemma actin sheet contributes not only to cell shape but also to cell locomotion.