New Scientist - USA (2022-04-02)

18 | New Scientist | 2 April 2022

Technology

Chris Stokel-Walker

A ROBOT trained by a machine-

learning algorithm that imitates

a human demonstrator can

successfully peel a banana without

smashing it to smithereens.

Handling soft fruit is a challenge

for robots, which often lack the

dexterity and nuanced touch to

process items without destroying

them. The uneven shape of fruit –

which can vary significantly even

with the same type of fruit – can

also flummox the computer-vision

algorithms that often act as the

brains of such robots.

Heecheol Kim at the University

of Tokyo and his colleagues have

developed a machine-learning

system that powers a robot

(pictured below), which has

two arms and hands that grasp

between two “fingers”.

It was trained by having a human

operating the robot peel hundreds

of bananas, creating 811 minutes

of demonstration data for the

system to learn from. After training,

the robot was able to successfully

peel a banana 57 per cent of the

time (arxiv.org/abs/2203.09749).

“What is really interesting in

this case is that the process that

a human uses has been carried

over into the training of the robot

system through the deep-imitation

learning,” says Jonathan Aitken

at the University of Sheffield, UK.

Aitken would like to see how

the robot handles fruit that is more

misshapen. The technology won’t

simply be used for bananas, though:

the goal is to train a system that

can deal with general tasks that

require fine motor skills. ❚

Robot works out

how to carefully

peel a banana

News

Medicine

Carissa Wong

TWO existing drugs may help

regenerate mouse lungs that

have been damaged by cigarette

smoke. The preliminary

findings suggest the drugs might

benefit people with chronic

obstructive pulmonary disease,

which currently has no cure.

COPD is the third leading

cause of death worldwide after

heart disease and stroke, and

can result from smoking, air

pollution or genetics. It involves

an excessive immune response

that irreversibly damages the

lungs, leading to elevated

mucus levels in them, shortness

of breath and chest tightness.

“The problem with COPD at

the moment is that we do not

have a way of preventing the

progression of disease and

the decline in lung function.

We only have ways to treat

symptoms,” says Reinoud

Gosens at the University of

Groningen in the Netherlands.

COPD damages so-called

epithelial progenitor cells that

normally regenerate the lining

of the lungs, meaning they

cannot repair themselves.

Previous efforts at treating this

condition have mainly focused

on invasive cellular therapies

such as stem cell implants,

which provide a source of

progenitor cells.

Gosens and his colleagues

analysed data previously

collected from the lung tissue

of people with COPD and mice

exposed to cigarette smoke, as

well as data from healthy people

and mice, to find out which

genes were more or less active

in diseased tissues compared

with healthy controls.

This allowed them to identify

two proteins in epithelial

progenitor cells that contributed

to the disease and could be

targeted with two existing

drugs: iloprost, which is used

to treat high blood pressure in

lung arteries, and misoprostol,

used to heal stomach ulcers.

To test these drugs, the team

exposed mice to cigarette

smoke for four months. Lung

progenitor cells were then

extracted from the animals

and grown in a gel for 14 days,

in dishes that each contained

one of the drugs, or control

dishes with no drug.

“You take the progenitor

cells and place them in a gel,

then they form these mini-lung

structures known as organoids,”

says Gosens. By assessing how

many organoids developed in

the absence or presence of the

drugs, the team found that both

drugs appeared to fully restore

the regenerative ability of the

progenitor cells, which declined

after exposure to the smoke.

The team also treated the

mice with the drugs during

a week of cigarette smoke

exposure and found they had

the same beneficial effect on

subsequently extracted lung

progenitor cells (Science

Advances, doi.org/hm24).

“Compared to other

drugs that can support lung

regeneration in animals,

the big benefit of the drugs

we’ve identified is that they’re

already used to treat other

conditions, so we know that

they are safe and they are

similarly effective,” says Gosens.

“I’m really delighted to see

people working on regenerative

power using drugs in COPD,”

says Rolf Ziesche at the Medical

University of Vienna, Austria.

“However, the model uses

mice aged at about 20 human

years, whereas typical COPD

patients are around 50 and

we know regenerative power

slows with age. Better models

are needed to really establish

therapeutic potential.” ❚

For more on regeneration,

see page 35

Drugs seem to help repair

damaged mouse lungs

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