I am a Cell Biologist with a particular interest in cells in connective tissue - specifically cartilage and bone. While there is already extensive research in this area, my approach is rather novel and is to study the cells in their natural environment i.e. within their 'extracellular matrix' which surrounds them in the intact tissues in our bodies. I have been particularly interested in using advanced microscopical methods (confocal scanning laser microscopy) because we can label the cells while they are in the tissue, and study their behaviour with minimal perturbation. While much of my work is directed towards basic properties of normal healthy cells, untimately I aim to understand the changes that initiate and cause the progression of common disorders of cartilage - especially osteoarthritis (OA). This is a very common debilitating disorder of the joints caused by the loss of cartilage matrix, and there is increasing evidence that this is not caused by 'wear-and-tear' but due to specific defects in which cartilage cells play a key role. Thus, while it might not be possible to 'cure' OA, there is good reason to think that cartilage can be protected against OA, but if it is initiated, then its progress can be significantly inhibited.

BSc (Physiology - class 2.1; 1976). University of Aberdeen

PhD (1981) Title: ‘The effects of high hydrostatic pressure on red blood cells’. Supervisor; Dr A.G. Macdonald. University of Aberdeen.

http://www.ed.ac.uk/integrative-physiology/staff-profiles/research-groups/andrew-hall

1. How can we protect cartilage cells against iatrogenic injury? During orthopaedic surgery, cartilage may be damaged through accident or design. This can kill healthy cartilage cells (chondrocytes) which are essential for the maintenance of normal resilient cartilage. We are studying the effects of the composition of the standard irrigation fluid which is used during surgery (normal saline) to see if we can give greater protection. Our studies show that raising the osmotic pressure of the saline (using sucrose) can markedly protect the cartilage cells and may accelerate cartilage repair.  We are also looking at the effects of cartilage drying on chondrocyte viability and attempting to clarify the mechanisms of cell death.

2. What is the role of cartilage cells (chondrocytes) in osteoarthritis (OA)? Osteoarthritis (OA) is an increasingly common, painful and debilitating disease of human articular cartilage. It used to be thought that it arose from cartilage ‘wear-and-tear’, resulting in loss of cartilage until bone rubs on bone which is exceedingly painful. However, there is increasing evidence that changes to the physiology of chondrocytes plays a key role, although the details are largely unclear. We have observed that there are marked changes to the shape of cartilage cells before there is any OA. We have seen that about 40% of the cells in otherwise healthy cartilage develop long, thin, cytoplasmic processes, and these are not normally present. This suggests that there are small but highly important changes to the chondrocytes which might represent the earliest stages of OA.

3. How can we protect cartilage against the damaging effects of Septic arthritis (SA)? Septic arthritis is a medical emergency and is caused by bacterial infection of the joint. The most common bacteria is Staphylococcus aureus, and it produces a range of potent and damaging toxins, some of which can kill cartilage cells. This leads to cartilage weakening and eventually osteoarthritis. It is clearly important to treat SA as quickly as possible but there is disagreement about the most effective antibacterials to use. We are currently identifying the key toxins produced by S. aureus, and testing various pharmacological agents for their ability to inhibit S. aureus growth and the production of toxins. 

4. Other areas of research interest include: signalling mechanisms in cell volume regulation, chondrocyte hypertropy in the growth plate, effect of cartilage injury on chondrocytes and culture of chondrocytes and factors influencing cell shape.

My research groups at present are small but focus on two areas: (a) protection of chondrocytes against iatrogenic injury and development of cartilage models (Dr A. Karim, Dr A. Amin) (b) chondrocyte morphology (Dr A. Karim, Dr A. Amin, Dr P. Bush), and (c) development of appropriate drug treatment for septic arthritis (Mr G. Hall, Prof. H. Simpson).

I routinely accept Honours (Intercalated medical Sciences BSc; Physiology Honours) students for projects. I also offer 20 week research projects for MSc Biomedical Sciences students. Unfortunately I have no funded positions at the present time.

Our work on protecting chondrocytes against injury ('chondroprotection') has been reported:28/01/15: (The Herald) (Daily Express) (Edinburgh Evening News) (Phy Org) (Daily Mail) (World Biomedical Frontiers). 

I collaborate with Orthopaedic surgeons at the Department of Orthopaedics and Trauma (University of Edinburgh; Dr. A. Amin, Prof. H. Simpson), Prof. Farquharson (skeletal development - Roslin Institute, University of Edinburgh) and Dr P. Bush (chondrocyte morphology - University of Sussex). 

I give lectures and run practical classes for Undergraduate Science and MBChB students for all years. I am Programme Director for the MSc Biomedical Sciences Programme. Various teaching/seminars/discussion sessions for postgraduate students.

• Director for postgraduate training and research in the Deanery of Biomedical Sciences.
• Member of the Board of Examiners for the College of Medicine and Veterinary Medicine
• Associate Director of Postgraduate Studies (PGR) for the College of Medicine & Veterinary Medicine.
• Convenor of the IMPACT (Image Analysis Multiphoton and Confocal Technologies) Imaging Committee.
• Director and lecturer for the Locomotor module (MBChB yr 1) and Director for Cell Communication theme (MSc Biomed. Sci.).
• Personal Tutor for approx. 20 undergraduate students, and a similar number of postgraduate students.