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Indian Origin Researcher part of Team that developed Automated Robotic Drill, will perform Surgery in 2.5 minutes

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Doctors performing surgery on a patient., Wikimedia

New York, May 1, 2017: A computer-driven automated drill that could perform a type of complex cranial surgery 50 times faster — decreasing the operating time from two hours to 2.5 minutes — has been developed by researchers, including one of the Indian-origin.

A translabyrinthine surgery is performed to expose slow-growing, benign tumours that form around the auditory nerves.

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For such complex surgeries, surgeons typically use hand drills to make intricate openings, adding hours to a procedure and may also increase the risks of loss of facial movement.

However, the new automated machine replaces hand drills to produce fast, clean, and safe cuts, reducing the time the wound is open and the patient is anesthetised, thereby decreasing the incidence of infection, human error, and surgical cost.

“I was interested in developing a low-cost drill that could do a lot of the grunt work to reduce surgeon fatigue,” said A.K. Balaji, Associate Professor at the University of Utah in the US.

The drill, which could play a pivotal role in future surgical procedures like hip implants, was developed from scratch to meet the needs of the neurosurgical unit, as well as developed software that sets a safe cutting path, the researchers said in the paper reported in the journal Neurosurgical Focus.

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First, the patient is imaged using a CT scan to gather bone data and identify the exact location of sensitive structures, such as nerves and major veins and arteries that must be avoided. Surgeons use this information to programme the cutting path of the drill.

In addition, the surgeon can programme safety barriers along the cutting path within 1 mm of sensitive structures.

If the drill gets too close to the facial nerve and irritation is monitored during surgery, the drill automatically turns off. (IANS)

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Researchers Identify New Mechanism to Prevent Alzheimer’s

The team next plans to test this approach in additional animal studies and eventually in human trials using small molecule inhibitors targeting eEF2K

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In Alzheimer's disease, patients start losing memory, Pixabay

Researchers have identified a novel mechanism and a potential new therapeutic target for Alzheimer’s disease (AD), says a new study on mice.

Alzheimer’s is characterised by profound memory loss and synaptic failure. Although the exact cause of the disease remains unclear, it is well established that maintaining memory and synaptic plasticity requires protein synthesis.

The function of the synapse is to transfer electric activity (information) from one cell to another.

“Alzheimer’s is such a devastating disease and currently there is no cure or effective therapy for it,” said Tao Ma, Assistant Professor at Wake Forest School of Medicine in the US.

A lady suffering from Alzheimer’s. Flickr

“All completed clinical trials of new drugs have failed, so there is clearly a need for novel therapeutic targets for potential treatments.”

For the study, the team has shown that AD-associated activation of a signaling molecule termed eEF2K leads to inhibition of protein synthesis.

Further, they wanted to determine if suppression of eEF2K could improve protein synthesis capacity, consequently alleviating the cognitive and synaptic impairments associated with the disease.

They used a genetic approach to repress the activity of eEF2K in Alzheimer’s mouse models.

Cognitive Impairment
Alzheimer’s disease patient Isidora Tomaz, 82, sits in an armchair in her house in Lisbon, Portugal. VOA

The findings, published in the Journal of Clinical Investigation, showed that genetic suppression of eEF2K prevented memory loss in those animal models and significantly improved synaptic function.

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“These findings are encouraging and provide a new pathway for further research,” said Ma.

The team next plans to test this approach in additional animal studies and eventually in human trials using small molecule inhibitors targeting eEF2K. (IANS)