Implantable electronics are among the most promising healthcare technologies, as they can help to remotely monitor specific biological processes associated with a patient’s health. While researchers have developed a variety of implantable devices over the past decade or so, existing technologies have several limitations that can prevent their widespread use in clinical settings.

The first factor preventing the large-scale implementation of existing implantable technologies is the structural mismatch between these devices and most organs/tissues in the body, which typically have complex 1D or 3D structures. Secondly, reliably fixing soft electronic devices on organs that are moving or pulsating has so far proved to be highly challenging.

Researchers at Daegu-Gyeongbuk Institute of Science & Technology (DGIST) in South Korea and ETH Zürich have recently developed a new fiber-based strain-sensing device that could overcome the limitations of existing implantable electronics. This sensor, presented in a paper published in Nature Electronics, comprises a capacitive fiber strain sensor with an inductive coil for wireless readout.

In diabetic nephropathy—a common cause of kidney disease—levels of NEDD4-2 are severely reduced. This is the case even when salt is not a factor.

University of South Australia researchers have identified an enzyme that may help to curb chronic kidney disease, which affects approximately 700 million people worldwide.

This enzyme, NEDD4-2, is critical for kidney health, says UniSA Centre for Cancer Biology scientist Dr. Jantina Manning in a new paper published this month in Cell Death & Disease.

The early career researcher and her colleagues, including 2020 SA Scientist of the Year Professor Sharad Kumar, have shown in an animal study the correlation between a high salt diet, low levels of NEDD4-2 and advanced kidney disease.

“In atopic dermatitis, the itching can be horrific, and it can aggravate disease,” said co-corresponding author K. Frank Austen, MD, a senior physician in the Division of Allergy and Clinical Immunology at the Brigham.

Scientists pinpointed a key molecular player that could represent a new therapeutic target for intractable chronic itch.