Currently the main treatment is a knee replacement, but this is only available to those with end-stage disease – meaning sufferers face up to 20 years of pain and impaired mobility.

The need for a replacement can be delayed by a high tibial osteotomy (HTO), a procedure where a surgeon makes an incision into the shin bone to realign the joint then stabilises it with a metal plate. In their current form, HTOs are lengthy, complex procedures, and also carry a risk to structures such as ligaments within the knee.

TOKA – a new treatment created by Professor Richie Gill from our Department of Mechanical Engineering and Centre for Therapeutic Innovation and ORTHOSCAPE, a medtech company based at the University's Innovation Centre – aims to change this. It uses CT scans to create a computerised 3D model of the patient’s anatomy, which acts as a digital guide for the procedure. Crucially, it’s also used to design and 3D-print a plate that precisely fits the recipient.

This tailored technology has been tested on 25 patients at the Rizzoli Orthopaedic Centre in Bologna, Italy, with incredibly promising results. “The doctors have said that the surgery is much better,” Richie explains. “The alignment they achieve is excellent, they can do the surgery in less than 30 minutes and, most importantly, all the patients have recovered quickly.”

The project is about to enter a randomised clinical trial in the UK, and the team are hopeful that TOKA will be widely available in the next few years. “The Italian patients all now, within six months of their surgery, want their other knee done with the same technology,” says Richie. “That’s a remarkable result, because the pain of the recent surgery usually makes people wait at least a year before considering further operations!”

They originate when DNA in stem cells of the epidermis – the outermost, protective layer of the skin – is damaged by the Sun’s radiation. Stem cells create copies of themselves through cell division, but also replenish mature cells as they die off. Issues arise when the balance between these two processes goes awry and stem cells divide more often than they should.

“Most of the work in our cells is done by proteins, and the instructions for how to make proteins come from genes,” says Dr Gernot Walko from the Department of Biology and Biochemistry and Cancer Research at Bath. “The process by which the information in a gene is turned into a functional protein is called gene expression. Only a fraction of the genes in a cell are expressed at any one time.”

He continues: “YAP/TAZ work in the cell’s nucleus, where they interact with many other proteins to promote the expression of genes that allow cells to divide. The problem comes when YAP/ TAZ are more active than they should be, enabling normal cells to become cancer cells.”

Gernot’s team – including PhD scholar Jodie Bojko, who is supported by alumnus Raoul Hughes (BSc Business Administration 1987) and his wife Catherine – are working on identifying the proteins that interact with YAP/TAZ specifically in cancer cells to cause this harmful overactivity. He continues: “We hope to identify proteins where drugs already exist or are in development, which can be used to treat YAP/ TAZ-driven tumours.”

Targeting these proteins rather than YAP/TAZ directly also means that their normal function of repairing and renewing the skin won’t be inhibited. These treatments could offer hope for a cure for various YAP/TAZ-driven cancers that avoids many of the unpleasant side effects of current therapies.

When you inhale, your heart beats slightly faster, slowing down again when you exhale. However, conventional pacemakers keep the heart beating at a fixed rate.

Professor Alain Nogaret from our Department of Physics is using artificial nerve cells – otherwise known as neurons – to create a ‘smart’ bionic pacemaker, which will help the heart to beat in a more natural rhythm by listening to signals from the body. This will enable the cardiac muscle to work more efficiently, addressing the symptoms of heart failure.

The artificial neurons are created by studying the signals sent by nerve cells in the brain. These parameters are then programmed to a silicon chip, which will replicate what nerve cells do naturally. “This allows us to resynchronise the heart rate to biological rhythms – in particular to respiration and blood pressure, but also oxygen and carbon dioxide concentration in the blood,” says Alain. “As a result, the heart saves energy and as it works more efficiently it is able to repair itself.”

Amazingly, the pacemaker has been shown in the lab to improve cardiac output by 17%, and to actually reverse the decay of cells in the heart muscle, says Alain. This is particularly promising because there is currently no cure available for heart failure, a condition that can ultimately prove fatal. Human studies are set to take place later this year in New Zealand. Alain continues: “We have proven the principle and, beyond any doubt, that restoring heart natural rate variability has major benefits for heart failure.”

A team led by Professor Jody Mason from our Department of Biology & Biochemistry have discovered a series of protein structures that are highly relevant to the onset of Parkinson’s disease.

The protein – alpha-synuclein (αS) – is abundant in all human brains, and the scientists are examining how they can form toxic deposits. These kill cells, causing dementia symptoms – and preventing their formation could help to keep brain cells healthier for longer. “Sometimes, when these proteins are produced, instead of getting to the right structure, they go rogue, ’misfolding’ and ending up in the wrong place,” says Jody. “Rather like plates stacking, they grow into very long toxic chains, which we call αS fibres.”

He is carrying out research to identify proteins that can bind to αS and prevent this toxic misfolding from occurring. The team are doing so by introducing millions of peptides – microscopic proteins just 10 amino acids (the building block of proteins) long – to αS inside living cells, and observing whether fibres form. This will also allow them to check if the peptides kill off cells – an obviously undesirable side effect.

“We’ve also been making step by step changes to the amino acids within the peptides; this involves going through the molecule to establish which of the 10 amino acids are talking to the target,” Jody explains. “If you can do that, then you can start to rationally design the peptide’s sequence to make it more effective and drug-like.” It’s hoped that this research will lead to future treatments for a disease that currently has no cure.

Without that sensation of touch, how can you tell how much pressure you’re exerting or how tightly you need to grip something? This challenge in prothesis development leaves many users frustrated, relying on their remaining limb and risking painful ‘overuse syndrome’.

Using electrical currents to stimulate nerves can produce a ‘feeling’ that is perceived as originating from the prosthesis, but so far, the method requires electrodes to be implanted into the arm. Not only is this invasive – and has the potential for infection – it also means that users aren’t able to test out the system before committing to it.

Electrical & Electronic Engineering PhD student Leen Jabban is developing a non-invasive system by attaching electrodes to the skin around the arm to target specific nerves. So far, she has achieved sensation in the ‘hand’ through electrical currents to the forearm, and is working on localising the stimulation.

“I aim to create a simple, cheap system that a user could fit themselves,” says Leen, whose scholarship is supported by alumnus Eur Ing Dr Brian Nicholson QC (PhD Electrical & Electronic Engineering 1998; Hon DEng 2018), Tony Best (Hon DEng 2013), and the Esther Parkin Trust. She is also the recipient of an Alumni Fund grant. “I’d like my research to be available to as many people as possible, so even those in the remotest parts of the world can access technology to help them live easier and healthier lives.”