Whether music delivered through
headphones or earbuds plays a role
in the increased hearing loss remains
unknown, but the new findings may trigger research into those devices, she says.
Using family income data, the
researchers also found that children living below the poverty line were more
likely to have hearing loss than were kids
above the line, but only in the 2005–2006
analysis. “One hypothesis is that poor
people have more untreated middle ear
infections,” says Yuri Agrawal, an otolaryngologist at Johns Hopkins University
School of Medicine in Baltimore who
wasn’t involved in the study. Such infections sometimes damage the inner ear
and sabotage hearing, she says.
Or, she says, the poverty may result
from poor hearing, not cause it. Families
with mildly poor hearing that is genetically passed on to the children may be
impoverished in part because hearing
loss can interfere with education and
achievement. “This can translate into
less opportunity and lower income-earning potential,” Agrawal says.
to get sick won’t need to take anti-TB
drugs that can damage the liver.
Courtesy of J.C. Bruusgaard/university of oslo
TB’s molecular signature was distinct from the gene profiles in blood
taken from people with other infectious diseases such as Streptococcus or
Staphylococcus, the researchers found.
The discovery was unexpected, as most
researchers thought that different types
of bacteria might change the activity of
specific genes at the site of the infection but that those differences would
not show up in the blood, says Andrea
Cooper, an infectious disease immunologist at the Trudeau Institute in Sara-nac Lake, N. Y. The variety of signatures
indicates that the immune system has
developed multiple ways of dealing with
infectious organisms.
“It highlights the beauty of the immune
response and its finesse in dealing with
different pathogens,” Cooper says.
18
percent
Hearing loss
rate among
adults 45–64
30
percent
Hearing loss
rate among
adults 65–74
47
percent
Hearing loss rate
among adults 75
and older
Muscles can remember past glory
nuclei made in training survive disuse, making regrowth easier
By Tina Hesman Saey
Pumping up is easier for people who
have been buff before, and now scientists
think they know why — muscles retain a
memory of their former fitness even as
they wither from lack of use.
That memory is stored as DNA-con-taining nuclei, which proliferate when a
muscle is exercised. Contrary to previous thinking, those nuclei
aren’t lost when muscles
atrophy, researchers
report online August 16
in the Proceedings of the
National Academy of Sciences. The extra nuclei
form a type of muscle
memory that allows the
muscle to bounce back
quickly when retrained.
The findings suggest that
exercise early in life could
help fend off frailness in
the elderly, says study
leader Kristian Gundersen,
a physiologist at the University of Oslo in Norway.
Because muscle cells are
huge, more than one nucleus is needed
to supply the DNA templates for making large amounts of the proteins that
give the tissue its strength. Previous
research has demonstrated that with
exercise, muscle cells get even bigger
by merging with stem cells called satellite cells, which are nestled between
muscle fiber cells. Researchers had
previously thought that when muscles
atrophy, the extra cell nuclei are killed
by a cell death program called apoptosis.
In the new study, Gundersen’s team
simulated the effect of working out by
making a muscle that helps lift the toes
work harder in mice. As the muscle
worked, the number of nuclei increased,
starting on day six. Over the course
of 21 days, the hard-working muscle
increased the number of nuclei in fiber
cells by about 54 percent. Starting on
day nine, the muscle cells also started
to plump up. Those results indicate that
the nuclei come first and muscle mass is
added later.
In another set of experiments, the
researchers worked the mice’s muscles
for two weeks and then severed nerves
so the muscle tissue would
atrophy. As it did, the cells
deflated to about 40 percent of their bulked-up
size, but the number of
nuclei in the cells did
not change.
These results contradict previous studies that
show lots of cell death in
muscles during atrophy.
Gundersen’s team examined individual cells in
the wasting muscles and
found that apoptosis is
going on, but that other
cells are dying, not the
muscle fibers or their
extra nuclei. The extra
nuclei stick around for at least three
months—a long time for a mouse,
which lives a couple of years on average,
Gundersen says.
“I don’t know if it lasts forever,” he
says, “but it seems to be a very long-lasting effect.” Since the extra nuclei
don’t die, they could be poised to make
muscle proteins again, providing a type
of muscle memory, he says.
“That’s fascinating thinking, and
there’s nice proof in this article to
support it,” says Bengt Saltin, a muscle physiologist at the University of
Copenhagen. “It’s really novel and
helps to explain descriptive findings
that muscles are quick to respond upon
further training.”
Training produces nuclei
(green) in muscle that
may help in rebuilding
strength after inactivity.
