News 22 juli 2009
Babies understand dog-speak, BYU
study finds
New research shows babies have a handle on the meaning of different dog barks –
despite little or no previous exposure to dogs. Infants just 6 months old can match the
sounds of an angry snarl and a friendly yap to photos of dogs displaying threatening and
welcoming body language. The new findings come on the heels of a study from the same
Brigham Young University lab showing that infants can detect mood swings in Beethoven’s
music. Though the mix of dogs and babies sounds silly, experiments of this kind help us
understand how babies learn so rapidly. Long before they master speech, babies recognize
and respond to the tone of what’s going on around them. “Emotion is one of the
first things babies pick up on in their social world,” said BYU psychology professor
Ross Flom, lead author of the study.
Future of Western Water Supply
Threatened by Climate Change, Says New CU-Boulder Study
As the West warms, a drier Colorado River system could see as much as a one-in-two chance
of fully depleting all of its reservoir storage by mid-century assuming current management
practices continue on course, according to a new University of Colorado at Boulder study.
The study, in press in the American Geophysical Union journal, Water Resources Research,
looked at the effects of a range of reductions in Colorado River stream flow on future
reservoir levels and the implications of different management strategies. Roughly 30
million people depend on the Colorado River -- which hosts more than a dozen dams along
its 1,450 journey from Colorado's Rocky Mountains to the Gulf of California -- for
drinking and irrigation water. The Colorado River system is presently enduring its 10th
year in a drought that began in 2000, said lead study author Balaji Rajagopalan, a
CU-Boulder associate professor of civil, environmental and architectural engineering.
Fortunately, the river system entered the drought with the reservoirs at approximately 95
percent of capacity. The reservoir system is presently at 59 percent of capacity, about
the same as this time last year, said Rajagopalan, also a fellow at CU-Boulder's
Cooperative Institute for Research in Environmental Sciences. The research team examined
the future vulnerability of the system to water supply variability coupled with projected
changes in water demand. The team found that through 2026, the risk of fully depleting
reservoir storage in any given year remains below 10 percent under any scenario of climate
fluctuation or management alternative. During this period, the reservoir storage could
even recover from its current low level, according to the researchers. But if climate
change results in a 10 percent reduction in the Colorado River's average stream flow as
some recent studies predict, the chances of fully depleting reservoir storage will exceed
25 percent by 2057, according to the study. If climate change results in a 20 percent
reduction, the chances of fully depleting reservoir storage will exceed 50 percent by
2057, Rajagopalan said.
UCLA researchers discover new
molecular pathway for targeting cancer, disease
A UCLA study has identified a way to turn off a key signaling pathway involved in
physiological processes that can also stimulate the development of cancer and other
diseases. The findings may lead to new treatments and targeted drugs using this approach.
In the study, which is currently available in the online edition of the journal Molecular
Endocrinology, scientists found that by activating a receptor in cells called the liver X
receptor (LXR), they were able to inhibit the hedgehog (Hh) signaling pathway, which is
involved in the maintenance of tissue integrity and stem cell generation. When stimulated
in an unregulated manner, however, the Hh pathway can also cause cancers of the brain,
lung, blood, prostate, skin and other tissues. Blocking such unregulated stimulation of
the Hh pathway had previously been shown in animal studies to prevent cancers, according
to the researchers. How LXR was able to inhibit tumor cell growth by impeding the Hh
pathway was previously unknown. "Our finding shows that activation of LXR signaling
is a novel strategy for inhibiting Hh pathway activity and for targeting various cell
types, including cancer cells, which may provide important clues as to how we might be
able to intervene with tumor formation," said Farhad Parhami, a professor of medicine
at the David Geffen School of Medicine at UCLA and the study's principal investigator.
During the study, researchers performed various tests activating LXR receptors in cells
and found that specific gene expression induced by the Hh pathway could be inhibited. This
finding was also confirmed in mice. "Since Hh signaling plays a major role in other
physiological and pathological processes, we may be able to impact other diseases as
well," Parhami said. Dr. William Matsui of Johns Hopkins Medical Institute, an expert
on Hh signaling in cancer development, noted the importance of the UCLA study and its
significance for the next stages of research — finding a pharmaceutical drug or
substance molecule to act as an agonist, which would stimulate LXR activity to inhibit
aberrant Hh signaling.
C. difficile spores spread superbug
New research suggests that antibiotic treatment could be asymptomatically inducing the
transmission of the healthcare-acquired infection, C. difficile, contributing to the
outbreaks that have recently been widely reported in hospitals and other settings. A team
of scientists have successfully mirrored the infection cycle of C. difficile by generating
a 'mouse hospital' with conditions mimicking the human environment in which C. difficile
is transmitted. The results have implications for infection control measures in the
healthcare environment and open the door for the development of treatments and improved
diagnosis of C. difficile. At present, healthcare professionals manage the threat of C.
difficile by observing stringent hygiene and isolation practices primarily by dealing with
patients who exhibit the symptoms of infection - including diarrhoea and fever. But
today's publication suggests that widening the targets of infection control in hospitals,
to include all patients receiving antibiotic treatment - although logistically complex -
is worth investigating. "C. difficile is a highly resistant and highly infectious
pathogen and resistant to many front line antibiotics," explains Dr Trevor Lawley,
Wellcome Trust Sanger Institute researcher and lead author on the study. "Until now,
animal studies have focussed on the observable, acute symptoms of C. difficile. But, to
understand how this highly infectious pathogen spreads, investigating the entire cycle of
transmission is absolutely vital. We looked at mice carrying C. difficile and observed
that they shed low levels of spores and, crucially, they did not infect other mice."
"But when we treated mice with antibiotics, we saw a dramatic rise in the levels of
spores shed - leading to what we have described as a 'supershedder state' and transmission
of C. difficile among mice. Importantly, transmission occurs even in the absence of
clinical symptoms." C. difficile transmission relies on the shedding of highly
resistant spores in the faeces of humans. These bacterial spores are essentially dormant
cells with protective outer layers making them well-adapted for survival and dispersal in
a wide range of environmental conditions. When humans shed spores in their faeces, those
spores are capable of surviving dormant in the environment for long periods of time, under
harsh conditions and in temperatures up to 70 ºC, before reintroduction and infection in
a new human host.
Breast cancer drug shows promise
against serious infections
An FDA-approved drug used for preventing recurrence of breast cancer shows promise in
fighting life-threatening fungal infections common in immune-compromised patients, such as
infants born prematurely and patients with cancer. Some scientists suspected that
tamoxifen has antifungal properties; now new research from the University of Rochester
Medical Center shows that it actually kills fungus cells and stops them from causing
disease. "It's still early, but if tamoxifen, or molecules like it, turns out to be
an effective treatment against serious fungal infections, it'll be a welcome addition to
our arsenal," said Damian Krysan, M.D., Ph.D., author of the research recently
published in the journal Antimicrobial Agents and Chemotherapy and assistant professor of
Pediatrics at the University of Rochester Medical Center . While serious fungal infections
are generally isolated to patients with cancer, patients in intensive care units, patients
with HIV or patients taking immune-suppression medications for chronic conditions, they
are among the deadliest infections. Fungus is the third most common cause of blood stream
infection in premature infants in the neonatal intensive care unit. The survival rate for
children with acute lymphoblastic leukemia is about 95 percent, but if they acquire a
Candida albicans fungal infection, that drops to 80 percent. Bacterial meningitis has a 5
percent risk of death, but the risk of death for C. albicans blood stream infection is 20
percent.
Research sheds light on cause of
Down syndrome and other genetic disorders
Scientists have a better understanding of what causes an abnormal number of chromosomes in
offspring, a condition called aneuploidy that encompasses the most common genetic
disorders in humans, such as Down syndrome, and is a leading cause of pregnancy loss. To
pinpoint what goes awry in these cases, researchers at the U.S. Department of Energy’s
Lawrence Berkeley National Laboratory and the University of Tennessee, Knoxville studied
mice. They found that if a mother’s egg cell has a mutation in just one copy of a
gene, called Bub1, then she is more likely to have fewer offspring that survive to birth.
Ordinarily, both copies of a gene in a chromosome must carry the same mutation in order
for an organism to be adversely effected. “But we found that a mutation in a single
copy of the Bub1 gene can have an impact — and this is not the case with most genes.
With Bub1, if you have one bad gene and one healthy gene, there’s a problem,”
says Francesco Marchetti of Berkeley Lab’s Life Sciences Division. He worked with
Sundaresan Venkatachalam of the University of Tennessee and other scientists on the
research. Their findings appear in the online early edition of the Proceedings of the
National Academy of Sciences the week of July 13.
Pregnancy complications are a
stress test for future maternal health and pregnancies
Predicting whether pregnancy complications affect long-term maternal health as well as
future pregnancies is at the heart of two studies conducted by researchers in the
Department of Obstetrics, Gynecology and Reproductive Sciences at Yale School of Medicine.
The first study, published in the journal Hypertension, showed that women who have had two
pregnancies complicated by preeclampsia are at a higher risk of hypertension after
pregnancy. Working in collaboration with the University of Copenhagen in Denmark, senior
author Michael Paidas, M.D., and his team conducted a retrospective study of over 11
million women who gave birth in Denmark from 1978 to 2007. Their findings showed that
among women with preeclampsia, a complication of pregnancy linked to life-threatening
cardiovascular disease, the risks of subsequent hypertension risks were compounded with
each affected pregnancy. Only healthy women without any other previously identified
medical problems were included in the study. "The only reliable treatment for
preeclampsia is delivery of the baby," said Paidas, associate professor and
co-director of Yale Women and Children's Center for Blood Disorders, Department of
Obstetrics, Gynecology & Reproductive Sciences. "But while delivery may 'cure'
preeclampsia in the moment, these mothers are at high risk of chronic hypertension, type 2
diabetes mellitus and blood clots for the rest of their lives. Pregnancy acts like a
natural stress test for women." Paidas said the research adds to growing data on the
link between hypertensive pregnancy disorders, diabetes, cardiovascular disease and
maternal death. Paidas and the research team are conducting ongoing studies to explore the
genetic links between pregnancy complications, cardiovascular disease and diabetes.
"Physicians and other healthcare professionals should be encouraged to include the
history of a woman's pregnancy outcomes when estimating the risk of cardiovascular
disease," said Paidas. "Identifying women soon after a hypertensive pregnancy
will alert care providers to the increased risks of heart disease, diabetes and blood
clotting and allow prompt intervention." In light of this new information, Paidas
also urges care providers to exercise caution when prescribing oral contraceptives to
women with hypertensive pregnancy complications.
Risk factors for cardiovascular
disease increasing in younger Canadians
The prevalence of heart disease and certain key risk factors – hypertension,
diabetes, and obesity – are increasing in all age groups and most income groups in
Canada found a new study published in CMAJ (Canadian Medical Association Journal). This
study, which looked at national data from 1994 to 2005, encompassed people aged 12 years
and older sampling from Canadians of all socioeconomic and ethnic groups. Risk factors
such as hypertension, diabetes, and obesity increased most rapidly among younger people
between 12 to 50 years of age. The increasing prevalence of heart disease in Canada is
likely related to both earlier detection and better survival among those with
cardiovascular disease. More Canadians are surviving their first heart attack. The
prevalence of heart disease is rising fastest among Canadians of lower socioeconomic
status, who also tend to have the highest cardiovascular risk profiles. This increase in
risk factors in younger Canadians has significant health implications because it
predisposes people to earlier onset heart disease. It can place greater burden on health
care resources as younger people may need longer, and perhaps more intense, treatment. The
study found an estimated 1.29 million Canadians reported having heart disease in 2005, a
19.3% increase in men and 2.1% increase in women compared with 1994. Although people who
were of lower socioeconomic status had the highest risk factor burden, hypertension
prevalence nearly doubled and obesity increased over time in all socioeconomic groups.
Diabetes is also increasing in almost all income groups, although the gap between the
richest and the poorest is widening over time.
Reveal the enemy
Bacterial diseases are usually detected by first enriching samples, then separating,
identifying, and counting the bacteria. This type of procedure usually takes at least two
days after arrival of the sample in the laboratory. Tests that work faster, in the field,
and without complex sample preparation, whilst being precise and error-free, are thus high
on the wish list. A Spanish research team headed by Jordi Riu and F. Xavier Rius at the
University Rovira i Virgili in Tarragona has now developed a new technique to make this
wish come true. With a novel biosensor, they have been able to detect extremely low
concentrations of the typhus-inducing Salmonella typhi. As reported in the journal
Angewandte Chemie, their new method is based on electrochemical measurements by means of
carbon nanotubes equipped with aptamers as bacteria-specific binding sites. If bacteria
bind to the aptamers, the researchers detect a change in electrical voltage. Aptamers are
synthetic, short DNA or RNA strands that can be designed and made to bind a specific
target molecule. An aptamer that specifically binds to salmonella has recently been
developed. The Spanish researchers chose to use this aptamer for their biosensor. By means
of additional functional groups, they securely anchored the aptamers to carbon nanotubes,
which were deposited onto an electrode in an ultrathin layer. In the absence of
salmonella, the aptamers fit closely against the walls of the carbon nanotubes. If the
biosensor is put into a salmonella-containing sample, the microbes stick to the aptamers
like flies to flypaper. This influences the interaction between the aptamers and the
nanotubes, which makes a change in the electrode voltage noticeable within seconds.
Children's IQ can be affected by
mother's exposure to urban air pollutants
Prenatal exposure to environmental pollutants known as polycyclic aromatic hydrocarbons
(PAHs) can adversely affect a child's intelligence quotient or IQ, according to new
research by the the Columbia Center for Children's Environmental Health (CCCEH) at the
Mailman School of Public Health. PAHs are chemicals released into the air from the burning
of coal, diesel, oil and gas, or other organic substances such as tobacco. In urban areas
motor vehicles are a major source of PAHs. The study findings are published in the August
2009 issue of Pediatrics. The study, funded by the National Institute of Environmental
Health Sciences (NIEHS), a component of the National Institutes of Health, the U.S.
Environmental Protection Agency and several private foundations, found that children
exposed to high levels of PAHs in New York City had full scale and verbal IQ scores that
were 4.31 and 4.67 points lower, respectively than those of less exposed children. High
PAH levels were defined as above the median of 2.26 nanograms per cubic meter (ng/m3).
"These findings are of concern because these decreases in IQ could be educationally
meaningful in terms of school performance," says Frederica Perera, DrPH, professor of
Environmental Health Sciences and director of the CCCEH at Columbia University Mailman
School of Public Health and study lead author. "The good news is that we have seen a
decline in air pollution exposure in our cohort since 1998, testifying to the importance
of policies to reduce traffic congestion and other sources of fossil fuel combustion
byproducts." The study included children who were born to non-smoking Black and
Dominican American women age 18 to 35 who resided in Washington Heights, Harlem or the
South Bronx in New York. The children were followed from in utero to 5 years of age. The
mothers wore personal air monitors during pregnancy to measure exposure to PAHs and they
responded to questionnaires.
Our brain looks at eyes first to
identify a face
A study by the University of Barcelona (UB) has analysed which facial features our brain
examines to identify faces. Our brain adapts in order to obtain the maximum amount of
information possible from each face and according to the study the key data for
identification come from, in the first place, the eyes and then the shape of the mouth and
nose. The objective of this study, undertaken by researcher Matthias S. Keil from the
Basic Psychology Department of the UB and published in the prestigious US journal PLoS
Computational Biology, was to ascertain which specific features the brain focuses on to
identify a face. It has been known for years that the brain primarily uses low spatial
frequencies to recognise faces. "Spatial frequencies" are, in a manner of
speaking, the elements that make up any given image.As Keil confirmed to SINC, "low
frequencies pertain to low resolution, that is, small changes of intensity in an image. In
contrast, high frequencies represent the details in an image. If we move away from an
image, we perceive increasingly less details, that is, the high spatial frequency
components, while low frequencies remain visible and are the last to disappear." As a
result of the psychophysical research carried out prior to the publication of this study,
it was known that the human brain was not interested in very high frequencies when
identifying faces, despite such frequencies playing a significant role in, for example,
determining a person's age. "In order to identify a face in an image, the brain
always processes information with the same low resolution, of about 30 by 30 pixels from
ear to ear, ignoring distance and the original resolution of the image," Keil says.
"Until now, nobody had been able to explain this peculiar phenomenon and that was my
starting point". What Matthias S. Keil did was to analyse a large number of faces,
namely those belonging to 868 women and 868 men. "The idea was to find common
statistical regularities in the images." Keil used a model of the brain's visual
system, that is, "I looked at the images to certain extent like the brain does, but
with one difference: I had no preferred resolution, but considered all spatial frequencies
as equal. As a result of this analysis, I obtained a resolution that is optimum in terms
of encoding, as well as the signal-to-noise ratio, and was also the same resolution
observed in the psychophysical experiments". This result therefore suggests that
faces are themselves responsible for our resolution preference. This led Keil to one of
the brain's properties: "The brain has adapted optimally to draw the most useful
information from faces in order to identify them. My model also predicts this resolution
if we take into account the eyes alone – ignoring the nose and the mouth – but
also by considering the mouth or nose separately, albeit less reliable."
Car horns warn against natural
disasters
In Batman's hometown of Gotham City, a gigantic searchlight projects the Bat signal into
the sky in case of disaster to alarm the superhero and the population. In Germany, an
extensive network of sirens was used in the past to warn the population against disasters:
in case of forest fires, industrial accidents or a looming inundation of a part of town,
civil protection agencies could trigger the loud and clear siren alarm, while detailed
information was provided by radio and television. However, after the end of the Cold War,
most sirens were dismantled in the mid-nineties to be replaced by the satellite-based
warning system SatWaS, which informs the population only via radio and television. But if
TV and radio are switched off, the warning goes unheard. In recent years, different
individual solutions for warning systems have been developed. Cell-broadcast systems can
send mass SMS messages to mobile phones. Smoke detectors, radio-controlled clocks and
weather stations equipped with radio receivers can also trigger alarm. Despite the high
distribution rate of some of these devices, it cannot be ensured that a warning reaches
the entire population. Only individual persons or households would be warned, and only if
the devices are on standby 24/7/365. Today, fire brigades and disaster protection agencies
would rather want the sirens back. However, the resulting costs would amount to several
100 million Euros for German federal and state governments, which share the responsibility
for civil protection. In January, researchers of the INT applied for a patent of a
technology which allows the horns of parked cars to be activated in case of disaster. The
technology is based on the eCall emergency system, which new cars are going to be equipped
with as from September 2010. The eCall system was developed at the initiative of the EU
Commission to help reduce the number of road traffic fatalities. It consists of a GPS
sensor and a mobile phone component, which is activated only in case of an accident (i.e.
when the airbags are triggered) and which can transmit data (e.g. accident time,
coordinates and driving direction of the vehicle) to an emergency call center.
Pacific tsunami threat greater than
expected
The potential for a huge Pacific Ocean tsunami on the West Coast of America may be greater
than previously thought, according to a new study of geological evidence along the Gulf of
Alaska coast. The new research suggests that future tsunamis could reach a scale far
beyond that suffered in the tsunami generated by the great 1964 Alaskan earthquake.
Official figures put the number of deaths caused by the earthquake at around 130: 114 in
Alaska and 16 in Oregon and California. The tsunami killed 35 people directly and caused
extensive damage in Alaska, British Columbia, and the US Pacific region*. The 1964 Alaskan
earthquake – the second biggest recorded in history with a magnitude of 9.2 –
triggered a series of massive waves with run up heights of as much as 12.7 metres in the
Alaskan Gulf region and 52 metres in the Shoup Bay submarine slide in Valdez Arm. The
study suggests that rupture of an even larger area than the 1964 rupture zone could create
an even bigger tsunami. Warning systems are in place on the west coast of North America
but the findings suggest a need for a review of evacuation plans in the region. The
research team from Durham University in the UK, the University of Utah and Plafker
Geohazard Consultants, gauged the extent of earthquakes over the last 2,000 years by
studying subsoil samples and sediment sequences at sites along the Alaskan coast. The team
radiocarbon-dated peat layers and sediments, and analysed the distribution of mud, sand
and peat within them. The results suggest that earthquakes in the region may rupture even
larger segments of the coast and sea floor than was previously thought. The study
published in the academic journal Quaternary Science Reviews and funded by the National
Science Foundation, NASA, and the US Geological Survey shows that the potential impact in
terms of tsunami generation, could be significantly greater if both the 800-km-long 1964
segment and the 250-km-long adjacent Yakataga segment to the east were to rupture
simultaneously. Lead author, Professor Ian Shennan, from Durham University's Geography
Department said: "Our radiocarbon-dated samples suggest that previous earthquakes
were fifteen per cent bigger in terms of the area affected than the 1964 event. This
historical evidence of widespread, simultaneous plate rupturing within the Alaskan region
has significant implications for the tsunami potential of the Gulf of Alaska and the
Pacific region as a whole. "Peat layers provide a clear picture of what's happened to
the Earth. Our data indicate that two major earthquakes have struck Alaska in the last
1,500 years and our findings show that a bigger earthquake and a more destructive tsunami
than the 1964 event are possible in the future. The region has been hit by large single
event earthquakes and tsunamis before, and our evidence indicates that multiple and more
extensive ruptures can happen."
Promising new treatment for
Alzheimer's suggested based on Hebrew University research
Research carried out at the Hebrew University of Jerusalem has resulted in a promising
approach to help treat Alzheimer's disease in a significant proportion of the population
that suffers from a particularly rapid development of this disease. In the research at the
Silberman Institute of Life Sciences of the Hebrew University, scientists solved a mystery
as to why people who carried a mutated gene known as BChE-K were prone to more rapid
development of Alzheimer's than those who had a normal version of the gene. This mutation
appears in about 20 percent of the American and Israeli populations. In theory, the
carriers of the mutated gene should actually be more protected from the devastating
effects of the disease, since the mutated protein (the enzyme that is the product of the
gene) breaks down the neurotransmitter acetylcholine at a slower rate than in those who
have the normal gene. The result is that the carriers maintain higher levels of this
neurotransmitter, so they should in principle be protected from Alzheimer's disease, in
which acetylcholine levels decrease. Indeed, these carriers tend to develop the disease
later than others, but when that happens, it progresses more rapidly and does not respond
to medication. Therefore, the bottom line is that carriers of the mutated gene have a
greater risk than others for disease progression. The reason for this anomalous situation
has been a puzzle for a long time, but the studies by the Hebrew University scientists
solved it by finding the explanation for this increased risk, thereby offering as well a
possible new therapeutic solution. At the Wolfson Center for Structural Biology at the
Hebrew University, the researchers found that the mutation in the BChE-K gene damages the
very end, or tail, of the resultant mutant enzyme protein. This tail is the part of BChE
which is important for protection from the Alzheimer's disease plaques. It does this by
interacting with the Alzheimer's disease ?-amyloid protein and preventing it from
precipitating and forming those brain plaques which are the neuropathological hallmark of
this disease. To compare the normal protein to the K mutant, the researchers used
synthetic tails of the normal and the K proteins, as well as engineered human BChE
produced in the milk of transgenic goats at a U.S. company, Pharmathene. The goat-
produced protein is prepared at Pharmathene for the U.S. military as protection from nerve
gas poisoning (a result of earlier research at the Hebrew University). It was much more
stable and efficient than the mutant protein, which suggests that the BChE-K carriers'
susceptibility to Alzheimer's could be substantially improved by treating them with the
engineered normal protein that is produced in the milk of the transgenic goats.
The right messenger for a healthy
immune response
Researchers from the Molecular Immunology group at the Helmholtz Centre for Infection
Research (HZI) in Braunschweig, Germany have now shown that Beta-Interferon also plays a
crucial role during an immune response: without Beta-Interferon immune cells are unable to
show "wanted posters" of pathogens to other cells. As a consequence, these cells
will not recognize the pathogen and the immune response does not start properly. The
group's results have now been published in the current issue of the scientific magazine
Journal of Immunology. During an infection, immune cells produce Beta-Inferferon.
Interestingly, an immune response is even stronger when a low amount of Beta-Interferon
has already been present before the infection occurs. Scientists call this behaviour
"priming". A healthy basal level of Beta-Interferon facilitates a faster immune
reaction against microbial and viral threads. Researchers from the HZI have now managed to
show why this is the case: Beta-Interferon is a key regulator and of vital importance in
enabling the immune system to display fragments of pathogens, so-called antigens. Immune
cells present these antigens on their surface and in this way communicate with one
another: antigens are the "wanted posters" of the virus or the bacterium which
has to be destroyed. The researchers discovered the important role of Beta-Interferon in
mice lacking the gene for Beta-Interferon. These mice displayed poor immune responses.
"Without those knock-out mice we would not have been able to identify the impact of
Beta-Interferon on the immune system," says Siegfried Weiß, leader of the Molecular
Immunology group at the HZI. His research assistant, the scientist Natalia Zietara,
investigated what Beta-Interferon is doing in immune cells. She found a molecular factor
that is pivotal in producing the pathogen's profile and which is regulated by
Beta-Interferon. The factor belongs to a group of proteins that is usually produced in
conditions of stress. Without Beta-Interferon, no active stress protein – without
stress protein, no wanted poster – without wanted poster, no immune response.
Gene linked to increasingly common
type of blood cancer
California and Arizona researchers have identified a gene variant that carries nearly
twice the risk of developing an increasingly common type of blood cancer, according to a
study published online today by the science journal Nature Genetics. Investigators at the
University of California, Berkeley (UC Berkeley) and at the Translational Genomics
Research Institute (TGen) found that mutations in a gene called C6orf15, or STG, are
associated with the risk of developing follicular lymphoma. This is a cancer of the body's
disease-fighting network whose rates have nearly doubled in the past three decades. In the
first genome-wide association study of non-Hodgkin lymphoma, scientists at UC Berkeley and
TGen identified a SNP – a single nucleotide polymorphism – that could determine
susceptibility to follicular lymphoma. The SNP, a DNA variant within the more than
3-billion base pairs in the human genome, was identified as rs6457327. The study was led
by Dr. Christine Skibola, Associate Adjunct Professor of Environmental Health Sciences at
UC Berkeley's School of Public Health, and by Dr. Kevin M. Brown, an Associate
Investigator in the Integrated Cancer Genomics Division of TGen, a Phoenix-based,
non-profit biomedical research institute. "What's exciting about this study is that
we found a target in the genome influencing the susceptibility to follicular lymphoma,
which helps us discern between three major types of lymphomas," said Skibola, the
paper's co-lead author. "That had not been done before on a genome-wide scale. It is
our hope that this research may some day be useful in helping develop prevention, early
detection and treatment of this disease."
Discovery of genetic toggle switch
inches closer to possible diabetes cure
Scientists have identified a master regulator gene for early embryonic development of the
pancreas and other organs, putting researchers closer to coaxing stem cells into
pancreatic cells as a possible cure for type1 diabetes. Researchers at Cincinnati
Children's Hospital Medical Center report their findings in the July 21 Developmental
Cell. Besides having important implications in diabetes research, the study offers new
insights into congenital birth defects involving the pancreas and biliary system by
concluding both organs share a common cellular ancestry in the early mouse embryo. This
discovery reverses a long standing belief that the biliary system's origin is connected to
early embryonic formation of the liver, the researchers said. The pancreas regulates
digestion and blood sugar, and the biliary system is vital for digestion. If the organs do
not form properly during fetal development, it can be fatal. The study reports that one
gene, Sox17 (a transcription factor that controls which genes are turned on or off in a
cell) is the key regulator for giving instruction to cells in early mouse embryos to
become either a pancreatic cell or part of the biliary system. The first author on the
paper is Jason Spence, Ph.D., a research fellow in the lab of the study's senior
investigator, James Wells, Ph.D., a researcher in the Division of Developmental Biology at
Cincinnati Children's and associate professor of pediatrics at the University of
Cincinnati College of Medicine. "We show that Sox17 acts like a toggle or binary
switch that sets off a cascade of genetic events," said Dr. Wells. "In normal
embryonic development, when you have an undecided cell, if Sox17 goes one way the cell
becomes part of the biliary system. If it goes the other way, the cell becomes part of the
pancreas." The finding advances ongoing research by Dr. Wells and his team to guide
embryonic stem cells to become pancreatic beta cells, which scientists believe could be
used to treat or cure type1 diabetes. The disease occurs when the immune system attacks
insulin producing beta cells in the pancreas, usually destroying them beyond repair before
the illness is diagnosed.
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