Research Round up
Less Sleep, Slower Performance
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Jeanne F. Duffy, PhD, MBA
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Researchers led by Jeanne F. Duffy, PhD, MBA, BWH associate neuroscientist, have
discovered that regardless of how tired a person thinks he or she is, lack of
sleep will still influence performance on certain tasks.
Researchers analyzed visual search task
results from 12 participants over a one month study conducted with the BWH
Center for Clinical Investigation. In the first week, participants were
scheduled to sleep 10 to12 hours per night to make sure they were well-rested.
For the following three weeks, the participants were scheduled to sleep the
equivalent of 5.6 hours per night, and also had their sleep times scheduled on
a 28-hour cycle, mirroring chronic jet lag.
The participants took computer tests that
involved visual search tasks, and how quickly they could find important
information. How accurate they were in identifying the information was recorded.
The longer the participants were awake, the
more slowly they identified the important information in the test. Also, during
the biological night time, 12 to 6 a.m., participants (who were unaware of the
time throughout the study) performed the tasks more slowly than they did during
the daytime. They also performed more slowly during each of the three
weeks when their nightly sleep was limited, although the participants'
self-ratings of sleepiness did not decline significantly over those same three
weeks.
"This research provides useful information
for workers who perform similar types of visual search tasks during the night
shift, because they will do it much more slowly than when they are working
during the day," said Duffy. "The longer someone is awake, the more their
ability to perform different tasks is hindered, and this impact is even
stronger at night. People who cut back on their sleep are often unaware of how
much their performance is impaired by sleepiness."
The study was published online in The Journal of Vision on July 26, 2012.
Cancers' Common Characteristics
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Raju Kucherlapati, PhD
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Raju
Kucherlapati, PhD, BWH Department of Medicine, principal investigator for the colon
cancer study of the Cancer Genome Atlas project, along with more than 200
scientists part of the multicenter research effort, have found genetic
vulnerabilities in colon cancer tumors that could lead to new treatments.
The researchers studied 224 tumors and saw
that aberrations in colon cancer tumors are also seen in other types of cancers
in the body. This finding could mean that drugs used to treat breast, skin and
other cancers may also be helpful in combating colon cancers.
For instance, about five percent of the colon
cancer tumors studied had extra copies of a gene called ERBB2. This
observation, also seen in many breast cancer tumors, led researchers to
hypothesize that a breast cancer drug called Herceptin, which targets ERBB2
genes, might also treat colon cancer. Future studies will help determine this.
Moreover, similar to previous studies, the researchers
found that about 15 percent of colon cancers had a mutation in the BRAF gene.
This gene is also mutated in melanoma. Researchers also discovered several
genetic pathways, such as one known as WNT that was mutated in 95 percent of
the colon cancer patients.
The study was published in the July 18, 2012
issue of Nature.
Cell Receptor has Proclivity for
T Helper 9 Cells, Airway Inflammation
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Xian Chang Li,
MD, PhD
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A research team led by Xian Chang Li, MD, PhD, BWH Transplantation Research Center, has
shed light on how a population of lymphocytes, called CD4+ T cells, mature into
various subsets of adult T helper cells. In particular, the team uncovered that
a particular cell-surface molecule, known as OX40, is a powerful inducer of new
T helper cells that make copious amounts of interleukin-9 (IL-9) (and therefore
called TH9 cells) in vitro; such TH9 cells are
responsible for ongoing inflammation in the airways in the lungs in vivo.
In their studies, the researchers found that
mice with hyper-active OX40 activities had signs of tissue inflammation,
particularly in tissues lining the airway. A high amount of cells-as much as 30
percent-in these tissues were mucin-producing cells. Mucin-producing cells make
gel-like secretions that, when combined with other secretions, can form mucus
or saliva.
"These findings may have broad impact on
how to treat chronic inflammation, such as allergic inflammation and chronic
allograft rejection after transplantation, since the inflammatory texture
organized by TH9 cells tends to be different and ongoing." said
Li.
Li and his team also made strides in better
understanding OX40's role in the molecular mechanisms of the pathway
responsible for TH9 cell induction.
According to Li, the revelation that OX40
promotes TH9 cells through TRAF6 (a protein that mediates cell
signaling) and the activation of a non-canonical NF-kB pathway will point to
new opportunities in drug discovery and development in treatment of TH9-related
diseases.
The study was published online in Nature Immunology on July 29, 2012.
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Francisco Quintana,
PhD
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Nanoparticles Play Part in Suppressing Autoimmune Disease
The immune response is normally controlled by
regulatory T cells. However, regulatory T cell deficits are usually found in
people with autoimmune disorders. A research team led by Francisco Quintana, PhD, BWH Department of Neurology, has
engineered nanoparticles that can serve as potential new tools for treating
autoimmune disorders by inducing regulatory T cells.
In the study, the researchers were able to
induce dendritic cells (immune cells that process antigens) to generate
regulatory T cells. They did this by using nanoparticles to deliver a small
molecule that activates a key transcription factor in dendritic cells together
with an antigen involved in central nervous system autoimmunity. This
nanoparticle delivery system was able to suppress development of experimental autoimmune
encephalomyelitis, an experimental model of multiple sclerosis.
"Nanoparticles constitute new tools to
co-deliver tissue-specific antigens and immunomodulatory small molecules to
re-establish antigen-specific tolerance in autoimmune diseases." said Quintana.
The study was published online in Proceedings of the National Academy of
Sciences on June 27, 2012.