Research briefs

Unblemished skin may be sun-damaged

A University of Queensland study has found skin with few visible freckles or blemishes may still carry sun-damaged DNA mutations that can trigger cancer.

Researchers investigated the relationship between the number of mutations found in ‘normal looking’ skin and the number of a person’s past skin cancers

Lead author and PhD candidate Ms Ho Yi Wong said the findings show Australians can have a high number of mutations in skin they think looks normal.

The study of skin samples from the forearms from 37 skin cancer patients had an average four to five times more mutations in normal-looking skin compared to similar studies overseas –possibly due to Australia having at least twice the amount of ultra-violet light than the United Kingdom and Europe.

The study next matched people of the same age and sex who had a different number of skin cancers and found a 45% difference between the groups, with a much larger number of mutations on the forearms of those with more skin cancers.

The findings explain in part why people with a single skin cancer have a much higher chance of developing others in the same area of the body.

Funding for detecting silicosis research

Monash University has secured funding of over $400,000 across two projects to improve early screening and detection of silicosis, an incurable and deadly occupational lung disease caused by breathing in silica dust.

The project aims to obtain a unique biochemical profile of the body’s response to silica, to develop a signature of ‘biomarkers’ in exhaled breath.

Monash Biomedicine Discovery Institute’s (BDI) Head of Respiratory Pharmacology Associate Professor Jane Bourke plans to test a number of drugs to reverse scarring of the lungs and has developed a model for testing silicosis drugs in human tissue.

‘We will take microscopic slices of tissue from human lungs, donated but not used for transplantation,’ she said. ‘We will expose them to silica dust and inflammatory protein cocktails found in the lungs of silicosis patients to cause lung damage and scarring.

‘This will mimic the environment in the silicotic lung. Then we can test two anti-fibrotic drugs (already approved and shown to be effective in another lung disease) and two promising novel in-house drugs to target inflammation and fibrosis in silicosis.’

Key to fighting inflammation in severe COVID-9 cases

A University of Queensland-led study into how immune cells respond to the COVID-19 virus is helping develop treatment to prevent runaway inflammation in patients with severe COVID-19.

The study found most immune cells which contribute to chronic inflammation are not infected with the SARS-CoV-2 virus. Uninfected cells - macrophages - detect damage and death in neighbouring cells and trigger a strong inflammatory response.

Anti-inflammatory drugs are currently given to hospitalised COVID-19 patients after the virus has peaked, to mitigate the overactive immune response but the drugs make patients susceptible to secondary infections.

The IMB research team is investigating how to selectively target macrophages without compromising the body’s ability to fight against the virus, in order to reduce the incidence of severe COVID.

With the new understanding of how macrophages work, the researchers aim to design anti-inflammatories that can be administered earlier, to prevent inflammation getting out of control.

The researchers say this is a way to future-proof against new variants of COVID-19 and also future pandemics and infections.

e-skin breakthrough

Scientists at UNSW Sydney have combined artificial synapses with advanced sensors to mimic the properties of human skin, in new research published in Advanced Functional Materials

Inspired by the human skin, researchers have developed an electronic device w able to detect mechanical stimuli for information processing, including gesture and handwriting recognition, with ultralow power consumption.

In biological nerve systems, sensory organs such as skin can detect stimuli and the generated signals can then be transmitted to the human brain via neurons and synapses for processing and eventually, response.

“People can feel pressure, pain, and interact with the surrounding environment through physical contact via the skin,” says Professor Dewei Chu, lead author of the study.

“Our system is proposed to mimic the functionality of the human skin, and several skin-like capabilities have been demonstrated.”

“The electric current that powers our device corresponds to the strength of the connection between two neurons. And we applied electric stimuli to control the device conductance to emulate human synaptic behaviours,” says Prof. Chu.

The complete system consists of the neuromorphic computing device, combined with highly responsive sensors.

The sensors can detect subtle human motion and monitor physiological signals.

Cure for MND closer

Research at The University of Queensland is a step closer to viable treatments, and ultimately a cure, for motor neuron disease (MND).

In their paper in Molecular Psychiatry, researchers have identified biochemical changes in a protein that is affected by MND.

They ran two research projects looking at how TDP-43 proteins, essential in the health of motor neurons, become dysfunctional.

They found diseased versions of TDP-43 can damage healthy versions of the protein, which may create a cycle of protein dysfunction and degeneration over time.

It also discovered that biochemical pathways which control neuron death are triggered early, even before MND symptoms begin.

The authors say pharmaceutical drugs that can prevent neuron death and this TDP-43 protein dysfunction are needed to change the course of the disease.

Researchers are now treating genetically modified mice with MND with different pharmaceutical drugs that specifically target the underlying causes of the disease, and correct the disease mechanism.

Arterial stiffness novel factor

Arterial stiffness may be a novel risk factor for metabolic syndrome in teens, a paper published in the American Journal of Physiology-Heart and Circulatory Physiology concludes.

Metabolic syndrome is the constellation of three or more of abdominal obesity, insulin resistance, hypertension, and hyperlipidemia. Metabolic syndrome increases the risk of worsening obesity, type 2 diabetes, cardiovascular disease, and premature death.

A new risk factor for childhood and adolescent metabolic disease such as obesity and insulin resistance is arterial stiffness. This risk factor is being established as a potential cause of type 2 diabetes among adults globally. However, it is not clear whether arterial stiffness causes metabolic syndrome.

The study of 3,862 adolescents aged 17 years who were followed up until age 24 years found worsening arterial stiffness was associated with a 9% risk of metabolic syndrome in males but no statistically significant risk among females.

Arterial stiffness potentially caused metabolic syndrome; however, metabolic syndrome did not cause arterial stiffness. The pathway through which arterial stiffness caused metabolism syndrome could be partly explained by an increase in fasting insulin (12% contribution) and low-density lipoprotein cholesterol (9% contribution).