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Revealed: Why smartphone batteries explode

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By NewsGram Staff Writer

The entire internal working of lithium-ion (Li-ion) batteries that leads to their overheating and exploding, has finally been revealed by scientists, according to a report published by Nature communications.

According to scientists, understanding how Li-ion batteries fail and potentially cause a chain reaction is important for improving their design and make them safer to use and transport.

Speaking on the experiment to study the Lithium batteries, Donal Finegan from University College London (UCL) said, “We combined high energy synchrotron X-rays and thermal imaging to map changes to the internal structure and external temperature of two types of Li-ion batteries as we exposed them to extreme levels of heat.”

The scientists exposed the battery shells to temperatures in excess of 250 degrees Celsius, and then looked at the effects of gas pockets formation, venting and increasing temperatures on the layers inside two distinct commercial Li-ion batteries

The battery with an internal support remained largely intact up until the initiation of thermal runaway, at which point the copper material inside the cell melted indicating temperatures up to 1,000 degrees Celsius.

This heat spread from the inside to the outside of the battery causing thermal runaway.

In contrast, the battery without an internal support exploded causing the entire cap of the battery to detach and its contents to eject.

Prior to thermal runaway, the tightly packed core collapsed, increasing the risk of severe internal short circuits and damage to neighbouring objects.

“Hopefully from using our method, the design of safety features of batteries can be evaluated and improved,” said corresponding author Paul Shearing, also from UCL.

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New Target For Parkinson’s Therapy Identified

The study revealed that, inside cells, alpha-synuclein binds to mitochondria, where cardiolipin resides

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The reason that Parkinson’s disease develops is not known. Wikimedia commons

Researchers have discovered one of the factors behind nerve cell death in Parkinson’s disease, unlocking the potential for new treatment to slow the progression of this fatal neurodegenerative disorder.

The researchers found that cardiolipin — a molecule inside nerve cells — helps ensure that a protein called alpha-synuclein folds properly. Misfolding of this protein leads to protein deposits that are the hallmark of Parkinson’s disease.

“Identifying the crucial role cardiolipin plays in keeping these proteins functional means cardiolipin may represent a new target for the development of therapies against Parkinson’s disease,” said Scott Ryan, Professor at the University of Guelph in Ontario, Canada.

“Currently there are no treatments that stop nerve cells from dying,” Ryan added.

ALSO READ: Testing Tears May Help In Early Diagnosis Of Parkinson’s Disease

These deposits are toxic to nerve cells that control voluntary movement. When too many of these deposits accumulate, nerve cells die, the researchers said.

For the study, published in the journal Nature Communications, researchers used stem cells collected from people with the disease. The team studied how nerve cells try to cope with misfolded alpha-synuclein.

10 million people living worldwide suffer from Parkinson;s disease Pixabay
10 million people living worldwide suffer from Parkinson’s disease. Pixabay

“We thought if we can better understand how cells normally fold alpha-synuclein, we may be able to exploit that process to dissolve these aggregates and slow the spread of the disease,” Ryan said.

The study revealed that, inside cells, alpha-synuclein binds to mitochondria, where cardiolipin resides. Cells use mitochondria to generate energy and drive metabolism.

ALSO READ: Progression of Parkinson disease could be slowed with exercise

Normally, cardiolipin in mitochondria pulls synuclein out of toxic protein deposits and refolds it into a non-toxic shape, the researchers added.

The researchers found that, in people with Parkinson’s disease, this process is overwhelmed over time and mitochondria are ultimately destroyed.

“As a result, the cells slowly die. Based on this finding, we now have a better understanding of why nerve cells die in Parkinson’s disease and how we might be able to intervene,” the researchers noted. (IANS)

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