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Week 35
New Strategy for Inhibiting Virus
Replication
Cellular protein as a new target for treatment of chronic hepatitis C / Virologists from
Heidelberg publish in PLoS Pathogens. Viruses need living cells for replication and
production of virus progeny. Thus far, antiviral therapy primarily targets viral factors
but often induces therapy resistance. New improved therapies attempt to targets cellular
factors that are essential for viral replication.The team led by Professor Dr. Ralf
Bartenschlager, Director of the Department of Molecular Virology at the Hygiene Institute
of Heidelberg University Hospital, has identified a protein in infected liver cells that
is essential for hepatitis C virus replication. Inhibiting this protein is highly
efficient in blocking virus replication. The study is to be published in the prestigious
journal Public Library of Science Pathogens.
Doing what the brain does - how
computers learn to listen
We see, hear and feel, and make sense of countless diverse, quickly changing stimuli in
our environment seemingly without effort. However, doing what our brains do with ease is
often an impossible task for computers. Researchers at the Leipzig Max Planck Institute
for Human Cognitive and Brain Sciences and the Wellcome Trust Centre for Neuroimaging in
London have now developed a mathematical model which could significantly improve the
automatic recognition and processing of spoken language. In the future, this kind of
algorithms which imitate brain mechanisms could help machines to perceive the world around
them. (PLoS Computational Biology, August 12th, 2009) Many people will have personal
experience of how difficult it is for computers to deal with spoken language. For example,
people who 'communicate' with automated telephone systems now commonly used by many
organisations need a great deal of patience. If you speak just a little too quickly or
slowly, if your pronunciation isn’t clear, or if there is background noise, the
system often fails to work properly. The reason for this is that until now the computer
programs that have been used rely on processes that are particularly sensitive to
perturbations. When computers process language, they primarily attempt to recognise
characteristic features in the frequencies of the voice in order to recognise words. 'It
is likely that the brain uses a different process', says Stefan Kiebel from the Leipzig
Max Planck Institute for Human Cognitive and Brain Sciences. The researcher presumes that
the analysis of temporal sequences plays an important role in this. 'Many perceptual
stimuli in our environment could be described as temporal sequences.' Music and spoken
language, for example, are comprised of sequences of different length which are
hierarchically ordered. According to the scientist’s hypothesis, the brain classifies
the various signals from the smallest, fast-changing components (e.g., single sound units
like 'e' or 'u') up to big, slow-changing elements (e.g., the topic). The significance of
the information at various temporal levels is probably much greater than previously
thought for the processing of perceptual stimuli. 'The brain permanently searches for
temporal structure in the environment in order to deduce what will happen next', the
scientist explains. In this way, the brain can, for example, often predict the next sound
units based on the slow-changing information. Thus, if the topic of conversation is the
hot summer, 'su…' will more likely be the beginning of the word 'sun' than the word
'supper'.
Proteins as resistance fighters
Friction limits the speed and efficiency of macroscopic engines. Is this also true for
nanomachines? A Dresden research team used laser tweezers to measure the friction between
a single motor protein molecule and its track. The team found that also within our cells,
motors work against the resistance of friction and are restrained in its
operation—usually by far not as much though as their macroscopic counterparts. These
first experimental measurements of protein friction could help researchers to better
understand key cellular processes such as cell division which is driven by such molecular
machines.
Raising the alarm when DNA goes bad
Our genome is constantly under attack from things like UV light and toxins, which can
damage or even break DNA strands and ultimately lead to cancer and other diseases.
Scientists have known for a long time that when DNA is damaged, a key enzyme sets off a
cellular ‘alarm bell’ to alert the cell to start the repair process, but until
recently little was known about how the cell detects and responds to this alarm. In a
study published today in Nature Structural and Molecular Biology, researchers at the
European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany, have identified a
whole family of proteins capable of a direct response to the alarm signal. Our genome is a
huge repository of information guiding the construction and function of all the cells in
our bodies. Cells sustain many hits to their DNA every day, which can lead tomutations, so
they maintain a fleet of DNA repair machinery that can be rapidly mobilised and sent to
damaged sites in an emergency.
Energy efficient sewage plants
High-rate digestion with microfiltration is state-of-the-art in large sewage plants. It
effectively removes accumulated sludge and produces biogas to generate energy. A study now
reveals that even small plants can benefit from this process. Sewage plants remove organic
matter from wastewater. If the accumulating sludge decays, biogas is generated as a
by-product. However, only 1156 of the 10,200 sewage plants in Germany have a digestion
tank. Smaller operations, especially, baulk at the costs of a new digestion tank. Instead,
they enrich the sludge with oxygen in the existing activation basin, and stabilize it.
“Activation basins require a lot of electricity. At the same time, enormous energy
potential is lost, since no biogas is produced,” says Dr. Brigitte Kempter-Regel of
the Fraunhofer Institute for Interfacial Engineering and Biotechnology IGB in Stuttgart.
“A sewage plant eats up more electricity in the municipalities than their hospitals
do”.
Cancer Mortality Rates Experience
Steady Decline
The number of cancer deaths has declined steadily in the last three decades. Although
younger people have experienced the steepest declines, all age groups have shown some
improvement, according to a recent report in Cancer Research, a journal of the American
Association for Cancer Research. “Our efforts against cancer, including prevention,
early detection and better treatment, have resulted in profound gains, but these gains are
often unappreciated by the public due to the way the data are usually reported,” said
Eric Kort, M.D., who completed the study while employed as a research scientist at Van
Andel Research Institute (VARI) in Grand Rapids, Mich. Cancer mortality rates are usually
reported as composite age-adjusted rates. These rates have been declining modestly since
the 1990's. However, these statistics heavily emphasize the experience of the oldest
Americans for whom mortality rates are the highest. As a result, trends emerging in
younger Americans can be concealed.
Sleep patterns in children and
teenagers could indicate risk for depression, researcher finds
Sleep patterns can help predict which adolescents might be at greatest risk for developing
depression, a researcher at UT Southwestern Medical Center has found in a five-year study.
Sleep is a biological factor known to be associated with adult depression. Depressed
adults experience rapid-eye-movement (REM) sleep earlier in the sleep cycle than people
who are not depressed. Until this study, available online and in the July edition of
Neuropsychopharmacology, it had been unclear whether this relationship held true in
adolescents. Dr. Uma Rao, professor of psychiatry at UT Southwestern and lead author of
the study, found that adolescents with a familial risk for depression but without a
depression diagnosis experienced shorter REM latency, meaning they reached the REM stage
more quickly. Those adolescents were more likely to develop depression by the end of the
five-year study period than those who reached REM sleep later in the cycle.“Sleep is
probably more helpful in determining who is at risk for developing depression than in
being a diagnostic marker for depression since REM latency of those adolescents was
shorter before they even developed the illness,” Dr. Rao said. Adolescent depression
is complex to prevent and to treat in part because baseline levels of sleep and other
factors used to diagnosis depression are not clearly defined. For example, in clinical
studies, adolescents without manifestation of mental illness can be labeled erroneously as
control group members because they haven’t yet reached the highest -risk period for
developing depression – mid- to late-adolescence and early adulthood.
Changes in net flow of ocean heat
correlate with past climate anomalies
Physicists at the University of Rochester have combed through data from satellites and
ocean buoys and found evidence that in the last 50 years, the net flow of heat into and
out of the oceans has changed direction three times. These shifts in the balance of heat
absorbed from the sun and radiated from the oceans correlate well with past anomalies that
have been associated with abrupt shifts in the earth's climate, say the researchers. These
anomalies include changes in normal storm intensities, unusual land temperatures, and a
large drop in salmon populations along the western United States. The physicists also say
these changes in ocean heat-flow direction should be taken into account when predicting
global climate because the oceans represent 90 percent of the total heat in the earth's
climate system. The study, which will appear in an upcoming issue of Physics Letters A,
differs from most previous studies in two ways, the researchers say. First, the physicists
look at the overall heat content of the Earth's climate system, measuring the net balance
of radiation from both the sun and Earth. And second, it analyzes more completely the data
sets the researchers believe are of the highest quality, and not those that are less
robust. "These shifts happened relatively abruptly," says David Douglass,
professor of physics at the University of Rochester, and co-author of the paper.
"One, for example, happened between 1976 and 1977, right when a number of other
climate-related phenomenona were happening, such as significant changes in U. S.
precipitation." Douglass says the last oceanic shift occurred about 10 years ago, and
that the oceans are currently emitting slightly more radiation than they are receiving.
Early fire use ignites discussion
about the evolution of human brainpower
New evidence that early modern humans used fire in southern Africa in a controlled way to
increase the quality and efficiency of stone tools is changing how researchers understand
the evolution of human behavior, and in particular, the evolution of human brain power.
Curtis Marean, a paleoanthropologist with the Institute of Human Origins at Arizona State
University, and an international team of researchers with members from South Africa,
England, Australia and France found 72,000-year-old, silcrete rocks that had been fired
and flaked to make stone tools in a cave along the coast of the southern tip of Africa in
Mossel Bay. The finding indicates that humans' ability to solve complex problems may have
occurred at the same time their modern genetic lineage appeared, rather than developing
later as has been widely speculated.
Active ingredients in marijuana
found to spread and prolong pain
Imagine that you're working on your back porch, hammering in a nail. Suddenly you slip and
hit your thumb instead — hard. The pain is incredibly intense, but it only lasts a
moment. After a few seconds (and a few unprintable words) you're ready to start hammering
again. How can such severe pain vanish so quickly? And why is it that other kinds of
equally terrible pain refuse to go away, and instead torment their victims for years?
University of Texas Medical Branch at Galveston researchers think they've found at least
part of the answer—and believe it or not, it's in a group of compounds that includes
the active ingredients in marijuana, the cannabinoids. Interestingly enough, given recent
interest in the medical use of marijuana for pain relief, experiments with rodents and
humans described in a paper published in the current issue of Science suggest these
"endocannabinoids," which are made within the human body, can actually amplify
and prolong pain rather than damping it down. "In the spinal cord there's a balance
of systems that control what information, including information about pain, is transmitted
to the brain," said UTMB professor Volker Neugebauer, one of the authors of the
Science article, along with UTMB senior research scientist Guangchen Ji and collaborators
from Switzerland, Hungary, Japan, Germany, France and Venezuela. "Excitatory systems
act like a car's accelerator, and inhibitory ones act like the brakes. What we found is
that in the spinal cord endocannabinoids can disable the brakes." To get to this
conclusion, the researchers began by studying what happened when they applied a
biochemical mimic of an endocannabinoid to inhibitory neurons (the brakes, in Neugebauer's
analogy) on slices of mouse spinal cord. Electrical signals that would ordinarily have
elicited an inhibitory response were ignored. They then repeated the procedure using
slices of spinal cord from mice genetically engineered to lack receptors where the
endocannabinoid molecules could dock, and found that in that case, the "brakes"
worked. Finally, using electron microscopy, they confirmed that the receptors were in fact
on inhibitory, not excitatory neurons. Endocannabinoids docking with them would suppress
the inhibitor neurons, and leave pain signals with a straight shot to the brain.
New findings show increased ocean
acidification in Alaska waters
The same things that make Alaska's marine waters among the most productive in the world
may also make them the most vulnerable to ocean acidification. According to new findings
by a University of Alaska Fairbanks scientist, Alaska's oceans are becoming increasingly
acidic, which could damage Alaska's king crab and salmon fisheries. This spring, chemical
oceanographer Jeremy Mathis returned from a cruise armed with seawater samples collected
from the depths of the Gulf of Alaska. When he tested the samples' acidity in his lab, the
results were higher than expected. They show that ocean acidification is likely more
severe and is happening more rapidly in Alaska than in tropical waters. The results also
matched his recent findings in the Chukchi and Bering Seas. "It seems like everywhere
we look in Alaska's coastal oceans, we see signs of increased ocean acidification,"
said Mathis. Often referred to as the "sister problem to climate change," ocean
acidification is a term to describe increasing acidity in the world's oceans. The ocean
absorbs carbon dioxide from the air. As the ocean absorbs more carbon dioxide, seawater
becomes more acidic. Scientists estimate that the ocean is 25 percent more acidic today
than it was 300 years ago. "The increasing acidification of Alaska waters could have
a destructive effect on all of our commercial fisheries. This is a problem that we have to
think about in terms of the next decade instead of the next century," said Mathis.
Study finds higher pathogen loads
in collapsed honeybee colonies
Honeybees in colonies affected by colony collapse disorder (CCD) have higher levels of
pathogens and are co-infected with a greater number of pathogens than their non-CCD
counterparts, but no individual pathogen can be singled out as the cause of CCD, according
to a study by an international team of researchers. The researchers, who represented Penn
State's College of Agricultural Sciences, University of Liege, Gembloux Agricultural
University, North Carolina State University and the U.S. Department of Agriculture's
Agricultural Research Service (ARS), collected samples of adult bees, wax comb, pollen and
brood – developing larvae – from 91 colonies in 13 apiaries in Florida and
California and quantified more than 200 variables, including the presence of parasites
such as varroa and tracheal mites; infection by bacteria, viruses and fungi; pesticide
levels; nutritional factors; and bee physiology. No single factor was found consistently
only in those colonies suffering from CCD. The study's findings, which were published in
the online journal PLoS ONE, illustrate the complexity of solving the CCD problem,
according to lead author and Penn State entomologist Dennis vanEngelsdorp. "Our
results suggest that this condition may be contagious or the result of exposure to a
common risk factor that impairs the bees' immune systems, making them more susceptible to
pathogens," said vanEngelsdorp, who also is acting state apiarist for the
Pennsylvania Department of Agriculture. VanEngelsdorp noted that higher pathogen loads are
likely to have caused CCD symptoms, but what causes the bees to become infected with so
many pathogens is still not known. "Although pathogens seem likely to play a critical
role in CCD, that role may be secondary, much like AIDS patients die from secondary
diseases," he added. No one of the screened pathogens had a higher prevalence in
colonies that had CCD. There also was no significant difference in the prevalence nor in
the total load of varroa or tracheal mites and Nosema, a protozoan that causes disease in
bees. But overall, CCD colonies were co-infected with a greater number of pathogens --
viruses, bacteria and microparasites such as Nosema. For instance, 55 percent of CCD
colonies were infected with three or more viruses compared to 28 percent of non-CCD
colonies. The researchers also found detectable levels of residues from 50 different
pesticides in all of the sampled colonies, but there was no association between increased
pesticide levels and CCD.
Mango seeds may protect against
deadly food bacteria
Life in the fruit bowl is no longer the pits, thanks to a University of Alberta
researcher. Christina Engels has found a way to turn the throwaway kernels in mangos into
a natural food preservative that could help prevent Listeriosis outbreaks like the one
that killed 21 Canadians last year. The findings can also apply to other fruit seeds like
grapes, said Engels, who conducted the research to earn her master's degree from the
Department of Agricultural, Food and Nutritional Science at the U of A. The research is
published in the latest Journal of Agricultural and Food Chemistry:
http://pubs.acs.org/doi/pdf/10.1021/jf901621m Pure tannins, a plant component extracted
from otherwise useless mango kernels by Engels, have proven inhibitory effects against
various strains of bacteria including Listeria, a potentially deadly pathogen that
infected some packaged meats and caused an outbreak of disease in Canada in 2008. Engels'
research focuses on a way to recycle wood-like mango kernels, which are usually thrown
away or burned. "By processing the kernels for their tannins, businesses have a way
to completely utilize all fruit parts and therefore increase their profit," she said.
Currently, mangos are one of the main fruits marketed globally, ranked fifth in world
production among the major fruit crops.
First human gene implicated in
regulating length of human sleep
Scientists have discovered the first gene involved in regulating the optimal length of
human sleep, offering a window into a key aspect of slumber, an enigmatic phenomenon that
is critical to human physical and mental health. The team, reporting in the Aug. 14, 2009
issue of Science, identified a mutated gene that allows two members of an extended family
to thrive on six hours of sleep a day rather than the eight to eight-and-a-half hours that
studies have shown humans need over time to maintain optimal health. Working from this
discovery, the scientists genetically engineered mice and fruit flies to express the
mutated gene and study its impact. While most Americans obtain less than eight hours of
sleep a night (the average on non-work days is 7.4 hours), and some may feel they succeed
with less when engaged in exhilarating work, domestic life or recreation, scientific
evidence indicates that, over time, the body suffers from this regimen, the researchers
say. "Short term and chronic disruptions in the length of optimal sleep can have
serious consequences on cognition, mood and physical health, including cancer and
endocrine function," says the senior author of the study, Ying-Hui Fu, PhD, UCSF
professor of neurology. However, teasing out this impact can be challenging, she says,
given access to such stimuli as coffee and chocolate. The finding, she says, offers an
opportunity to unravel the regulatory mechanism of sleep. While the mutation may be rare,
it could offer a probe more generally into the regulatory mechanisms of sleep quality and
quantity. Understanding these mechanisms could lead to interventions to alleviate
pathologies associated with sleep disturbance. Sleep remains a relatively inscrutable
biological phenomenon. Scientists know that it is regulated in large part by two
processes: 1) circadian rhythms -- genetic, biochemical and physiological mechanisms that
wax and wane during a 24 hour period to regulate the timing of sleep, 2) and homeostasis
– unknown mechanisms that ensure that the body acquires over time the necessary
amount of sleep, nudging it toward sleep when it has been deprived, prompting it out of
sleep when it has received enough. This regulation of sleep intensity is measured in non
rapid eye movement sleep and REM sleep. Interactions between the circadian rhythms and
homeostatic mechanisms influence the timing, duration and quality of sleep and
wakefulness. But "the details in the process are really completely unknown,"
says Fu.
Listening to rocks helps
researchers better understand earthquakes
When Apollo punished King Midas by giving him donkey ears, only the king and his barber
knew. Unable to keep a secret, the barber dug a hole, whispered into it, "King Midas
has donkey ears," and filled the hole. But plants sprouted from the hole, and with
each passing breeze, shared the king's secret. Earth, as it turns out, has other secrets
to divulge. From the pounding of the surf and the rumbling of thunder, to the gentle
rustling of leaves, Earth is not a quiet planet. The key is knowing how to listen to the
ever-present ambient noise. University of Illinois seismologist Xiaodong Song and graduate
student Zhen J. Xu have become good listeners, especially to the sounds beneath our feet.
Using a technique called "ambient noise correlation," Xu and Song have observed
significant changes in the behavior of parts of Earth's crust that were disturbed by three
major earthquakes. "The observations are important for understanding the aftermath of
a major earthquake at depth," Song said, "and for understanding how the rock
recovers from it and begins again to accumulate stress and strain for future
earthquakes." The pair report their findings in a paper accepted for publication in
the Proceedings of the National Academy of Sciences, and posted on the journal's Web site.
Researchers have used ambient noise to image Earth's interior and to monitor changes in
seismic velocity near active volcanoes.
New DNA Test Uses Nanotechnology to
Find Early Signs of Cancer
Using tiny crystals called quantum dots, Johns Hopkins researchers have developed a highly
sensitive test to look for DNA attachments that often are early warning signs of cancer.
This test, which detects both the presence and the quantity of certain DNA changes, could
alert people who are at risk of developing the disease and could tell doctors how well a
particular cancer treatment is working.The new test was reported in a paper called
“MS-qFRET: a quantum dot-based method for analysis of DNA methylation,”
published in the August issue of the journal Genome Research. The work also was presented
at a conference of the American Association of Cancer Research. “If it leads to early
detection of cancer, this test could have huge clinical implications,” said Jeff
Tza-Huei Wang, an associate professor of mechanical engineering whose lab team played a
leading role in developing the technique. “Doctors usually have the greatest success
in fighting cancer if they can treat it in its early stage.”
Developmental language disorders at
preschool age - no proof of benefit from screening
Language is a central element of social life. It is not only a prerequisite for personal
relationships, but also for employment prospects. If a child's language development is
impaired, this can have far-reaching negative consequences. Thus, it would be beneficial
if those children who would benefit from targeted help could be identified at a very early
stage. However, the Institute for Quality and Efficiency in Health Care (IQWiG) could not
find any proof of benefit from language screening before their 6th birthday for children
with a specific developmental disorder of speech and language. At present, there is a lack
of screening studies and also of reliable diagnostic instruments. This is the conclusion
in the final report, which IQWiG published on 17 August 2009.
Loose Change 9/11: An American Coup
Aspartame, Sweet Misery Documentary
The toxic long-term effects of aspartame
are often dismissed as a "hoax" by the sweetener industry and at least five
other internet websites. The real footwork, however, unravels something less comforting
than a mere "Hoax." "Sweet Misery" is the title of a documentary
released by Sound and Fury in June of 2004. Our primary investigation includes interviews
with doctors, lawyers, people who have had health problems which they associate with
aspartame usage, advocates, and many others
In the winter of 2006, a strange phenomenon
fell upon honeybee hives across the country. Without a trace, millions of bees vanished
from their hives. A precious pollinator of fruits and vegetables, the disappearing bees
left billions of dollars of crops at risk and threatened our food supply. The epidemic set
researchers scrambling to discover why honeybees were dying in record numbers — and
to stop the epidemic in its tracks before it spread further. Silence of the Bees is the
first in-depth look at the search to uncover what is killing the honeybee. The filmmakers
of Bees take viewers around the world to the sites of fallen hives, to high-tech labs,
where scientists race to uncover clues, and even deep inside honeybee colonies. Silence of
the Bees is the story of a riveting, ongoing investigation to save honeybees from dying
out. The film goes beyond the unsolved mystery to tell the story of the honeybee itself,
its invaluable impact on our diets and takes a look at whats at stake if honeybees
disappear. Silence of the Bees explores the complex world of the honeybee in crisis and
instills in viewers a sense of urgency to learn ways to help these extraordinary animals.
Innovators in the food industry are
building new connections in the supply chain to embrace the trend for local and organic
food. "Good Food, Good Business" features interviews with leaders in this trend
to help inform everyone from farmers and grocers to restauranteurs and educators.
How does the food lobby influence
obesity?
Rogan Kersh, Associate Professor of
Public Service and Associate Dean for Academic Affairs at NYU Wagner, discusses how the
food lobby influences obesity.
Sea of Trouble - Australia
A war is raging out there on the high seas
as the world's fishing stocks dwindle. Saddled with inadequate international fishing law
nations can do little to protect their fish from rogue vessels. For the mysterious Orange
Roughy it's a fight that could soon end in extinction.
Study supports DNA repair-blocker
research in cancer therapy
Scientists at Dana-Farber Cancer Institute have uncovered the mechanism behind a promising
new approach to cancer treatment: damaging cancer cells' DNA with potent drugs while
simultaneously preventing the cells from repairing themselves. The findings being reported
in the Aug. 14 issue of Molecular Cell help explain the promising results being seen in
clinical trials of compounds that force cancer cells with genetic damage to self-destruct
instead of "resting" while their DNA undergoes repairs. "What we have shown
suggests that you can use these drugs to sensitize cancer cells to DNA-damaging
chemotherapy," said Geoffrey Shapiro, MD, PhD, senior author of the report.
"This is a mechanism by which these inhibitory drugs may be synergistic with
DNA-damaging agents." Interestingly, Shapiro said, when the same repair-blocking
drugs were administered to normal, non-cancerous cells, the cells became less sensitive to
DNA damage from a chemotherapy drug. This is an encouraging indication that
repair-blocking drugs may selectively make cancer cells vulnerable to chemotherapy while
protecting normal cells from DNA damage, the scientists said. Cells' native capacity for
fixing DNA damage is normally beneficial, but it can be problematic for cancer therapy as
it enables tumor cells to become resistant to a number of standard drug agents. All cells
progress through a series of phases -- called the cell cycle -- including quiescence, or
resting, growth, and cell division. The transition from one phase to the next is regulated
by "checkpoint" proteins that, among other things, are designed to prevent
damaged, potentially dangerous cells from reproducing. The body deals with DNA-damaged
cells in two ways. It can order them to self-destruct through "programmed cell
death," also known as apoptosis. Or, it can issue signals from the checkpoint
proteins to put the cells into "cell cycle arrest," causing them to remain
quiescent while the broken DNA is fixed before they resume normal activity.
Children with headache
Family quarrels and a lack of free time can promote headaches in children. This is what
Jennifer Gassmann and her coauthors concluded in their study on risk factors, which
appears in the current issue of the Deutsches Ärzteblatt International (Dtsch Arztebl Int
2009; 106[31-32]: 509-16). This investigation was a component of a large-scale study
entitled "Children, Adolescents, and Headache" (Kinder, Jugendliche und
Kopfschmerz—KiJuKo), in which data were collected in four annual "waves"
from 2003 to 2006. Out of a multitude of variables tested in the larger study, the authors
chose to look at the ones that concerned the children's family and leisure time. Up to 30%
of all children around the world complain of headache symptoms arising at least once per
week. Boys who experienced more than one family quarrel per week had a 1.8 times higher
risk of developing headaches. The amount of free time available to them seemed to be even
more important: boys who only sometimes had time to themselves had a 2.1 times higher risk
of developing headaches. Parents' behavior when their child complains of headache also
seemed to play a major role. Either positive or negative reinforcement from the parents
teaches the child that he or she can gain certain advantages from headache symptoms. The
parents' responses had a particularly strong effect on the frequency of symptoms in girls:
reinforcing parental responses raised their risk of recurrent headaches by 25%. The sexes
also differed with respect to the frequency of headache. Twice as many girls as boys had
their symptoms at least once a week. The children's age, however, seemed to have no more
than a minor effect on headache manifestations.
Mother's immune system may block
fetal treatments for blood diseases
Pediatric researchers have resolved an apparent contradiction in the field of prenatal
cell transplantation— a medical approach that holds future promise in correcting
sickle cell disease and other serious congenital blood disorders. In a new study in
animals, the researchers showed that the mother's immune response interferes with the
offspring's earlier ability to tolerate transplanted donor cells. The study team concludes
that focusing on transplant techniques that avoid the maternal immune response may allow
scientists to take advantage of fetal tolerance to achieve a long-sought goal of treating
blood diseases prenatally. While cautioning that much work must be done to understand how
these animal findings apply to humans, the current findings are "surprising but
reassuring," said study leader Alan W. Flake, M.D., of the Children's Center for
Clinical Research at The Children's Hospital of Philadelphia. The study appeared online
August 3 in the Journal of Clinical Investigation. For over 50 years, explained Flake, it
has been a fundamental precept of immunology that a fetus tolerates foreign antigens in a
window-of-opportunity period before its immune system fully develops the capacity to mount
an immune response. Scientists assumed that by carefully introducing donor cells and
stimulating a fetus to develop tolerance to those cells, one could set the stage for a
later organ or cellular transplant that would not be rejected by a more mature immune
system. As prenatal diagnosis has continued to become available for a greater number of
congenital diseases, scientists have considered the possibility of correcting blood
disorders such as sickle cell disease or thalassemia. After first transplanting a small
number of healthy cells in an early-stage fetus to establish tolerance, a second dose of
transplanted cells later in gestation would proliferate, and treat the blood disorder
before birth. Researchers use hematopoietic cells—stem cells that that develop into
blood cells—in this technique, in utero hematopoietic cell transplantation (IUHCT).
However, over the years, Flake's team and other research groups found that IUHCT studies
in animal models yielded inconsistent results, ranging from no tolerance to transplants to
full tolerance and every degree of tolerance in between. Contrary to the concept of fetal
tolerance, an immune barrier seemed to be acting against transplanted cells.
Agricultural methods of early
civilizations may have altered global climate, study suggests
Massive burning of forests for agriculture thousands of years ago may have increased
atmospheric carbon dioxide enough to alter global climate and usher in a warming trend
that continues today, according to a new study that appears online Aug. 17 in the journal
Quaternary Science Reviews. Researchers at the University of Virginia and the University
of Maryland-Baltimore County say that today's 6 billion people use about 90 percent less
land per person for growing food than was used by far smaller populations early in the
development of civilization. Those early societies likely relied on slash-and-burn
techniques to clear large tracts of land for relatively small levels of food production.
"They used more land for farming because they had little incentive to maximize yield
from less land, and because there was plenty of forest to burn," said William
Ruddiman, the lead author and a professor emeritus of environmental sciences at the
University of Virginia. "They may have inadvertently altered the climate."
Ruddiman is a climate scientist who specializes in investigating ocean-sediment and
ice-core records. In recent years he has searched across scientific disciplines –
anthropology, archaeology, population dynamics, climatology – to gain insight into
how humans may have affected climate over the millennia. He said that early populations
likely used a land-clearing method that involved burning forests, then planting crop seed
among the dead stumps in the enriched soil. They would use a large plot until the yield
began to decline, and then would burn off another area of forest for planting. They would
continue this form of rotation farming, ever expanding the cleared areas as their
populations grew. They possibly cleared five or more times more land than they actually
farmed at any given time. It was only as populations grew much larger, and less land was
available for farming or for laying fallow, that societies adopted more intensive farming
techniques and slowly gained more food yield from less land.
Cancer's break-in tools possibly
identified at Duke
A single cell in a 1-millimeter nematode worm is providing valuable new clues into
cancer's deadliest behavior -- its ability to put down roots in new tissues after
spreading throughout the body. Duke University biologist David Sherwood has spent the last
several years studying the mechanics of a single cell in the developing body of a worm
called Caenorhabditis elegans. It's called the anchor cell and one of its jobs is to
connect the developing animal's uterus with its vulva, a crucial step in ensuring the
worm's fertility. To establish this slender connection, the anchor cell must work its way
through two layers of basement membrane, a dense, sheet-like barrier structure lining most
tissues, including the epithelial cells in humans that are the hosts of many cancers. In a
paper appearing online Aug. 17 in the journal Developmental Cell, Sherwood and colleagues
describe how the nematode's anchor cell uses a series of molecular signals to create a
stretched opening in the membrane. They believe the process is essentially the same as the
one cancer cells use to invade new tissues. Together, these molecules, called integrin and
netrin, may be a valuable new target in the efforts to halt cancer's spread via
metastasis.
Less than 50 percent of women with
abnormal paps receive follow-up care
Less than half of Ontario women with abnormal Pap tests receive recommended and
potentially life-saving follow-up care, according to a new women's health study by
researchers at St. Michael's Hospital and the Institute for Clinical Evaluative Sciences
(ICES). What's more, low-income women are less likely to be screened for cancer compared
to their high-income counterparts. "Cervical cancer is one of the most preventable
forms of cancer, yet in Ontario more than one million women have not been screened, and a
disproportionate number of these are women living in lower-income communities," says
Dr. Arlene Bierman, a physician at St. Michael's Hospital and principal investigator of
the Project for an Ontario Women's Health Evidence-Based Report (POWER). "We need to
make special efforts to reach women who are screened, but do not receive the necessary
follow-up and may eventually fall through the cracks. To improve surveillance and
treatment, we need a system that ensures all abnormal Pap tests are followed-up so that
Ontario women can receive the best care possible," added Dr. Bierman, a researcher at
ICES. The joint study titled POWER (the Project for an Ontario Women's Health
Evidence-Based Report), from St. Michael's Hospital and the Institute for Clinical
Evaluative Sciences (ICES), is the first in the province to provide a comprehensive
overview of women's health in relation to gender, income, education, ethnicity and
geography. The findings are detailed in the report titled Cancer — the second to be
released this year as part of the study. Findings can be used by policymakers and
health-care providers to improve access, quality and outcomes of care for Ontario women.
Dr. Monika Krzyzanowska, a medical oncologist at Princess Margaret Hospital/University
Health Network is the lead author on the cancer chapter. The POWER Study is funded by
Echo: Improving Women's Health in Ontario, an agency of the Ontario Ministry of Health and
Long-Term Care.
Diabetes drug linked to increased
risk of heart failure
Rosiglitazone, a drug used to treat type 2 diabetes, is associated with an increased risk
of heart failure and death among older patients compared to a similar drug (pioglitazone),
concludes a study published on bmj.com today. As such, the researchers say it is difficult
to advocate continued use of rosiglitazone for most patients. Rosiglitazone and
pioglitazone belong to a class of drugs called thiazolidinediones and are widely used for
the treatment of type 2 diabetes. They help to control blood sugar levels, but both drugs
can also cause side effects including weight gain, fluid retention and heart failure. It
is unclear whether there are clinically important differences in the cardiac safety of
these two drugs, so researchers in Canada compared the risk of heart attack, heart failure
and death in patients treated with rosiglitazone and pioglitazone. Using prescription
records, they identified nearly 40,000 patients aged 66 years and older who started
treatment with either rosiglitazone or pioglitazone between April 2002 and March 2008.
Data on hospital admission for either a heart attack or heart failure during the six-year
study period were recorded and deaths were identified from a national database.
Little known type of cholesterol
may pose the greatest heart disease risk
Health-conscious people know that high levels of total cholesterol and LDL cholesterol
(the so-called "bad" cholesterol) can increase the risk of heart attacks. Now
scientists are reporting that another form of cholesterol called oxycholesterol —
virtually unknown to the public — may be the most serious cardiovascular health
threat of all. Scientists from China presented one of the first studies on the
cholesterol-boosting effects of oxycholesterol here today at the 238th National Meeting of
the American Chemical Society. The researchers hope their findings raise public awareness
about oxycholesterol, including foods with the highest levels of the substance and other
foods that can combat oxycholesterol's effects. "Total cholesterol, low-density
lipoprotein cholesterol (LDL), and the heart-healthy high-density lipoprotein cholesterol
(HDL) are still important health issues," says study leader Zhen-Yu Chen, Ph.D., of
Chinese University of Hong Kong. "But the public should recognize that oxycholesterol
is also important and cannot be ignored. Our work demonstrated that oxycholesterol boosts
total cholesterol levels and promotes atherosclerosis ["hardening of the
arteries"] more than non-oxidized cholesterol." Fried and processed food,
particularly fast-food, contains high amounts of oxycholesterol. Avoiding these foods and
eating a diet that is rich in antioxidants, such as fresh fruits and vegetables, may help
reduce its levels in the body, the researchers note. Scientists have known for years that
a reaction between fats and oxygen, a process termed oxidation, produces oxycholesterol in
the body. Oxidation occurs, for instance, when fat-containing foods are heated, as in
frying chicken or grilling burgers or steaks. Food manufacturers produce oxycholesterol
intentionally in the form of oxidized oils such as trans-fatty acids and
partially-hydrogenated vegetable oils. When added to processed foods, those substances
improve texture, taste and stability. Until now, however, much of the research focused on
oxycholesterol's effects in damaging cells, DNA, and its biochemical effects in
contributing to atherosclerosis. Chen believes this is one of the first studies on
oxycholesterol's effects in raising blood cholesterol levels compared to non-oxidized
cholesterol. In the new study, Chen's group measured the effects of a diet high in
oxycholesterol on hamsters, often used as surrogates for humans in such research. Blood
cholesterol in hamsters fed oxycholesterol rose up to 22 percent more than hamsters eating
non-oxidized cholesterol. The oxycholesterol group showed greater deposition of
cholesterol in the lining of their arteries and a tendency to develop larger deposits of
cholesterol. These fatty deposits, called atherosclerotic plaques, increase the risk for
heart attack and stroke.
Plastics in oceans decompose,
release hazardous chemicals, surprising new study says
In the first study to look at what happens over the years to the billions of pounds of
plastic waste floating in the world’s oceans, scientists are reporting that plastics
— reputed to be virtually indestructible — decompose with surprising speed and
release potentially toxic substances into the water. Reporting here today at the 238th
National Meeting of the American Chemical Society (ACS), the researchers termed the
discovery “surprising.” Scientists always believed that plastics in the oceans
were unsightly, but a hazard mainly to marine animals that eat or become ensnared in
plastic objects. “Plastics in daily use are generally assumed to be quite
stable,” said study lead researcher Katsuhiko Saido, Ph.D. “We found that
plastic in the ocean actually decomposes as it is exposed to the rain and sun and other
environmental conditions, giving rise to yet another source of global contamination that
will continue into the future.”
'Housekeeping' genes play important
role in developmental pathways of cells
A study from the Center for Molecular Genetics at the University of California, San Diego
School of Medicine shows that a gene called HPRT plays an important role in setting the
program by which primitive or precursor cells decide to become normal nerve cells in the
human brain. This unconventional view of metabolic genes known as "housekeeping"
genes is now online at the journal Molecular Therapy. "Housekeeping" genes are
expressed in most cells under most conditions, and scientists usually regard them as
having simple metabolic functions that regulate normal metabolism, or that can cause
serious disease when the genes don't function properly. But they were not previous thought
to be involved with setting developmental pathways that determine how stem cells and other
primitive cells decide to become neurons, muscle cells, bone or blood cells ."We
showed that HPRT carries out an important new role by causing mistakes in the ways in
which a number of super-regulatory genes called transcription factors genes are expressed
– some up, some down, but many incorrectly," said Theodore Friedmann, MD,
professor of pediatrics and director of the Gene Therapy Program at the UC San Diego
School of Medicine. The researchers propose that many other housekeeping genes in addition
to HPRT may also be found to regulate important developmental pathways. The study also
provides the first direct experimental support for a possible role that HPRT plays in the
development of the devastating neurological disorder in Lesch Nyhan disease, a rare,
X-linked inherited disorder caused by a deficiency of an enzyme produced by mutations in
the HPRT gene. Complications of the disease usually appear in boys during their first year
of life, and may result in severe gout and kidney problems, poor muscle control, and
neurological problems that cause the boys to injure themselves uncontrollably. The study
by the Friedmann group now supports the idea that the HPRT gene defects cause neurological
problems by directly interfering with the birth and function of brain neurons, especially
the ones that rely on dopamine for nerve transmission.
How Meningitis Bacteria Attack the
Brain
A specific protein on the surface of a common bacterial pathogen allows the bacteria to
leave the bloodstream and enter the brain, initiating the deadly infection known as
meningitis. The new finding, which may guide development of improved vaccines to protect
those most vulnerable, including young infants and the elderly, is now available online in
the Journal of Experimental Medicine."Streptococcus pneumoniae, commonly known as
pneumococcus, is responsible for half the cases of bacterial meningitis in humans,"
said the study's senior author, Victor Nizet, MD, professor of pediatrics and pharmacy at
the University of California, San Diego’s School of Medicine and Skaggs School of
Pharmacy and Pharmaceutical Sciences. “As many as 30 percent of patients can die from
this rapidly progressing infection, while half of survivors may be left with permanent
neurological problems including deafness, seizures, intellectual deficits or motor
disabilities.”
Anti-Aging Gene Linked to High
Blood Pressure
Researchers at the University of Oklahoma Health Sciences Center have shown the first link
between a newly discovered anti-aging gene and high blood pressure. The results, which
appear this month in the journal Hypertension, offer new clues on how we age and how we
might live longer. Persistent hypertension, or high blood pressure, is a risk factor for
stroke, heart attack, heart failure, arterial aneurysm and is the leading cause of chronic
kidney failure. Even a modest elevation of arterial blood pressure leads to shortened life
expectancy. Researchers, led by principal investigator Zhongjie Sun, tested the effect of
an anti-aging gene called klotho on reducing hypertension. They found that by increasing
the expression of the gene in laboratory models, they not only stopped blood pressure from
continuing to rise, but succeeded in lowering it. Perhaps most impressive was the complete
reversal of kidney damage, which is associated with prolonged high blood pressure and
often leads to kidney failure. “One single injection of the klotho gene can reduce
hypertension for at least 12 weeks and possibly longer. Klotho is also available as a
protein and, conceivably, we could ingest it as a powder much like we do with protein
drinks,” said Sun, M.D., Ph.D., a cardiovascular expert at the OU College of
Medicine. Scientists have been working with the klotho gene and its link to aging since
1997 when it was discovered by Japanese scientists. This is the first study showing that a
decline in klotho protein level may be involved in the progression of hypertension and
kidney damage, Sun said. With age, the klotho level decreases while the prevalence of
hypertension increases.
Watching Stem Cells Repair the
Human Brain
There is no known cure for neurodegenerative diseases such as Huntington's, Alzheimer's
and Parkinson's. But new hope, in the form of stem cells created from the patient's own
bone marrow, can be found — and literally seen — in laboratories at Tel Aviv
University. Dr. Yoram Cohen of TAU's School of Chemistry has recently proven the viability
of these innovative stem cells, called mesenchymal stem cells, using in-vivo MRI. Dr.
Cohen has been able to track their progress within the brain, and initial studies indicate
they can identify unhealthy or damaged tissues, migrate to them, and potentially repair or
halt cell degeneration. His findings have been reported in the journal Stem Cells.
LSUHSC research discovers new
targets for treatment of invasive breast cancer
Research led by Suresh Alahari, PhD, Associate Professor of Biochemistry and Molecular
Biology at LSU Health Sciences Center New Orleans, has shown for the first time that a
tiny piece of RNA appears to play a major role in the development of invasive breast
cancer and identified a gene that appears to inhibit invasive breast cancer. The research
is published in the August 21, 2009 issue of the Journal of Biological Chemistry. The
LSUHSC researchers are the first to demonstrate that miR-27b, a novel microRNA, not only
inactivates the ST14 gene which they found suppresses the growth of breast tumor cells,
but also that miR-27b stimulates the breast cancer to invade other cells. MicroRNAs are a
new class of small, single-stranded RNA molecules which play an important regulatory role
in cell biology. They bind to target genes and decrease their function. MicroRNAs may act
as oncogenes (a gene that contributes to cancer development) or tumor suppressors. In this
study working with a line of human breast cancer cells, Dr. Alahari's team found that
aggressively invasive breast tumor cells contain a large quantity of miR-27b molecules,
while normal cells do not. Further analysis revealed that miR-27b increases during cancer
progression, in direct proportion to the decrease in function of the ST14 gene. They found
that miR-27b promotes cell growth and cell invasion, suggesting that miR-27b acts as a
breast cancer oncogene. They also found that ST14 inhibits both cell growth and cell
invasion, suggesting that ST14 is a breast cancer tumor suppressor gene and that it may
also serve as a marker for the early detection of breast cancer.
Progesterone leads to inflammation,
a breast cancer risk factor
Scientists at Michigan State University have found exposure to the hormone progesterone
activates genes that trigger inflammation in the mammary gland. This progesterone-induced
inflammation may be a key factor in increasing the risk of breast cancer. Progesterone is
a naturally occurring steroid hormone and promotes development of the normal mammary
gland. Progesterone previously has been identified as a risk factor for breast cancer, and
in a study published in the Journal of Steroid Biochemistry and Molecular Biology, MSU
scientists examined the genes activated by progesterone and the effects of their
activation in a mouse model system. Exposure to progesterone in normal amounts and in
normal circumstances causes inflammation, which promotes breast development. However,
exposure to progesterone in menopausal hormone therapy is known to increase breast cancer
risk. “Progesterone turns on a wide array of genes involved in several biological
processes, including cell adhesion, cell survival and inflammation,” said physiology
professor Sandra Haslam, co-author of the paper and director of the Breast Cancer and the
Environment Research Center at MSU. “All of these processes may be relevant to the
development of breast cancer.” The study shows progesterone significantly regulates
162 genes in pubertal cells, 104 genes in adult cells and 68 genes at both developmental
stages. A number of these genes make small proteins, called chemokines, which control the
process of inflammation.
Study reveals new metabolic
safeguards against tumor cells
Cells don't like to be alone. In the early stages of tumor formation, a cell might be
pushed out of its normal home environment due to excessive growth. But a cell normally
responds to this homeless state by dismantling its nucleus, packing up its DNA, and
offering itself to be eaten by immune system cells. Simply put, the homeless cell kills
itself. This process, known as apoptosis, typically stops potential cancer cells before
they have a chance to proliferate.Now, researchers from the lab of Harvard Medical School
professor of cell biology Joan Brugge have uncovered another mechanism that kills these
precancerous, homeless cells. By studying two different types of human breast epithelial
cells, the researchers found that when separated from their natural environment, these
cells lose their ability to harvest energy from their surroundings. Eventually, they
starve."We originally thought that in order for cells to survive outside their normal
environment, they would simply need to suppress apoptosis," says Brugge, senior
author on the paper, which will appear August 19 online in Nature. "But our studies
indicate that this activity is not sufficient to prevent the demise of homeless cells.
Even if they escape apoptosis, these cells can't transport enough glucose to sustain an
energy supply." Surprisingly, metabolic function is restored if antioxidant activity
is increased inside the cells, allowing the cells to use energy pathways that don't rely
on glucose. "It raises the interesting idea that antioxidants, which are typically
thought to be protective because they prevent genomic damage, might be allowing these
potentially dangerous cells to survive," says first author Zachary Schafer, assistant
professor at the University of Notre Dame and a former postdoc in Professor Brugge's lab.
New approach to wound healing may
be easy on skin, but hard on bacteria
In a presentation today (Aug. 19) to the American Chemical Society meeting, Ankit Agarwal,
a postdoctoral researcher at the University of Wisconsin-Madison, described an
experimental approach to wound healing that could take advantage of silver's
anti-bacterial properties, while sidestepping the damage silver can cause to cells needed
for healing. Silver is widely used to prevent bacterial contamination in wound dressings,
says Agarwal, "but these dressings deliver a very large load of silver, and that can
kill a lot of cells in the wound." Wound healing is a particular problem in diabetes,
where poor blood supply that inhibits healing can require amputations, and also in burn
wards. Agarwal says some burn surgeons avoid silver dressings despite their constant
concern with infection. Using a new approach, Agarwal has crafted an ultra-thin material
carrying a precise dose of silver. One square inch contains just 0.4 percent of the silver
that is found in the silver-treated antibacterial bandages now used in medicine. In tests
in lab dishes, the low concentration of silver killed 99.9999 percent of the bacteria but
did not damage cells called fibroblasts that are needed to repair a wound. Agarwal builds
the experimental material from polyelectrolyte multilayers — a sandwich of ultra-thin
polymers that adhere through electrical attraction. To make the sandwich, Agarwal
alternately dips a glass plate in two solutions of oppositely charged polymers, and
finally adds a precise dose of silver. "This architecture is very easily tuned to
different applications," Agarwal says, because it allows exact control of such
factors as thickness, porosity and silver content. The final sandwich may range from a few
nanometers to several hundred nanometers in thickness. (One nanometer is one-billionth of
a meter; a human hair is about 60,000 nanometers in diameter.) Nicholas Abbott, a
professor of chemical and biological engineering who advises Agarwal, says during the past
decade, "about a bazillion papers have been published on polyelectrolyte multilayers.
It's been a tremendous investment by material scientists, and that investment is now ripe
to be exploited."
Future angst? Brain scans show
uncertainty fuels anxiety
Anyone who has spent a sleepless night anguishing over a possible job loss has experienced
the central finding of a new brain scan study: Uncertainty makes a bad event feel even
worse. A new study by UW-Madison brain researcher Jack Nitschke shows that the emotional
centers in the brain respond much more strongly to disturbing photos if the person didn't
know what was coming.
Romantic, candle-lit dinners - An
unrecognized source of indoor air pollution
Burning candles made from paraffin wax –– the most common kind used to infuse
rooms with romantic ambiance, warmth, light, and fragrance –– is an unrecognized
source of exposure to indoor air pollution, including the known human carcinogens,
scientists reported here today. Levels can build up in closed rooms, and be reduced by
ventilation, they indicated in a study presented at the 238th National Meeting of the
American Chemical Society (ACS). In the study, R. Massoudi Ph.D., and Amid Hamidi , Ph.D.,
said that that candles made from bee's wax or soy, although more expensive, apparently are
healthier. They do not release potentially harmful amounts of indoor air pollutants while
retaining all of the warmth, ambience and fragrance of paraffin candles (which are made
from petroleum). "An occasional paraffin candle and its emissions will not likely
affect you," Hamidi said. "But lighting many paraffin candles every day for
years or lighting them frequently in an un-ventilated bathroom around a tub, for example,
may cause problems." Besides the more serious risks, he also suggested that some
people who believe they have an indoor allergy or respiratory irritation may in fact
actually be reacting to air pollutants from burning candles.
Scientists help explain effects of
ancient Chinese herbal formulas on heart health
New research at The University of Texas Health Science Center at Houston suggests that
ancient Chinese herbal formulas used primarily for cardiovascular indications including
heart disease may produce large amounts of artery-widening nitric oxide. Findings of the
preclinical study by scientists in the university's Brown Foundation Institute of
Molecular Medicine for the Prevention of Human Diseases (IMM) appear in the Sept. 15 print
issue of the journal Free Radical Biology & Medicine. Nitric oxide is crucial to the
cardiovascular system because it signals the inner walls of blood vessels to relax, which
facilitates the flow of blood through the heart and circulatory system. The messenger
molecule also eliminates dangerous clots, lowers high blood pressure and reduces
artery-clogging plaque formation. The results from this study reveal that ancient Chinese
herbal formulas "have profound nitric oxide bioactivity primarily through the
enhancement of nitric oxide in the inner walls of blood vessels, but also through their
ability to convert nitrite and nitrate into nitric oxide," said Nathan S. Bryan,
Ph.D., the study's senior author and an IMM assistant professor. Herbal formulas are a
major component of traditional Chinese medicines (TCMs), which also include acupuncture
and massage. "TCMs have provided leads to safe medications in cancer, cardiovascular
disease and diabetes," said C. Thomas Caskey, M.D., IMM director and CEO. "The
opportunity for Dr. Bryan's work is outstanding given that cardiac disease is the No. 1
cause of death in the United States." In the study, researchers performed laboratory
tests on DanShen, GuaLou and other herbs purchased at a Houston store to assess their
ability to produce nitric oxide. Ancient Chinese herbal formulas used primarily for
cardiovascular indications are made up of three to 25 herbs. The formulas can be
administered as tablets, elixirs, soups and teas.
How meningitis bacteria attack the
brain
A specific protein on the surface of a common bacterial pathogen allows the bacteria to
leave the bloodstream and enter the brain, initiating the deadly infection known as
meningitis. The new finding, which may guide development of improved vaccines to protect
those most vulnerable, including young infants and the elderly, is now available online in
the Journal of Experimental Medicine. "Streptococcus pneumoniae, commonly known as
pneumococcus, is responsible for half the cases of bacterial meningitis in humans,"
said the study's senior author, Victor Nizet, MD, professor of pediatrics and pharmacy at
the University of California, San Diego's School of Medicine and Skaggs School of Pharmacy
and Pharmaceutical Sciences. "As many as 30 percent of patients can die from this
rapidly progressing infection, while half of survivors may be left with permanent
neurological problems including deafness, seizures, intellectual deficits or motor
disabilities." Meningitis develops when bacteria penetrate the "blood-brain
barrier." Comprised of a single layer of highly specialized microvascular endothelial
cells, the blood-brain barrier prevents most large molecules from entering into the
cerebrospinal fluid, preserving an optimal biochemical environment for brain function. The
UC San Diego team investigated the functions of a protein known as NanA in order to
discover how an entire bacterium can breech the blood-brain barrier and gain access to the
central nervous system. NanA is produced by all strains of pneumococcus and displayed
prominently on the bacteria's outer surface. Through genetic manipulations, the
researchers were able to remove the entire NanA protein, or just specific sections of the
molecule, from the pathogen. They found that while normal pneumococci were able to bind,
enter and penetrate through human brain microvascular endothelial cells, mutant bacteria
lacking the NanA protein –or those expressing only a truncated version of the protein
– largely lost these abilities. Conversely, when the full-length pneumococcal NanA
protein was cloned and expressed on the surface of a nonpathogenic laboratory strain, the
transformed bacteria gained the ability to bind and enter the same endothelial cells.
Mutation in renin gene linked to
inherited kidney disease
A mutation in a gene that helps regulate high blood pressure is a cause of inherited
kidney disease, according to a new study by researchers at Wake Forest University School
of Medicine, Charles University in Prague and colleagues. The discovery provides insight
into a protein, renin, that is important in blood pressure regulation, and reveals the
cause of one type of inherited kidney disease occurring in adults and children, said
co-investigator Anthony Bleyer, M.D., professor of internal medicine-nephrology at the
School of Medicine. The study is now available online and in the Aug. 14 issue of American
Journal of Human Genetics. While more than 25,000 articles have been written about renin,
this is the first article to identify a mutation in the renin gene as a cause of kidney
disease. Renin is a key component of blood pressure regulation. When blood pressure drops,
kidney cells detect the change and release renin into the blood stream, where it converts
inactive forms of the hormone angiotensin into angiotensin I. With the help of a molecule
in the lungs called angiotensin-converting enzyme (ACE), angiotensin I is then converted
to a much more powerful hormone, called angiotensin II, which acts directly on blood
vessels to cause blood pressure increases. Because of the significant role renin plays, an
entire class of medications used to treat high blood pressure, called ACE inhibitors, are
dedicated to preventing blood pressure from rising by blocking the renin from activating
angiotensin. A genetic mutation in the gene that encodes renin was first identified as the
cause of an hereditary kidney disease by a research group led by Stanislav Kmoch, Ph.D.,
at Charles University in Prague. Working with Kmoch and Suzanne Hart, Ph.D., at the
National Institutes of Health, Bleyer identified the condition among American families in
his study group of families with rare, inherited kidney disease. Bleyer works with about
100 families throughout the world to identify the causes of inherited kidney disease that
run in their families. Families identified with the specific genetic mutation investigated
in this study suffer from anemia in childhood and progressive kidney disease resulting in
the need for dialysis, a mechanical way to cleanse the blood. Children typically have
relatively low blood pressure. Adults suffer from gout and worsening kidney disease.
Scripps Research, UCSD, and
University of Oslo team ties genetic variations to brain size
Using advanced brain imaging and genomics technologies, an international team of
researchers co-led by Scripps Research Institute scientists has shown for the first time
that natural variations in a specific gene influence brain structure. By establishing this
link, the researchers have opened the door to a range of potential research efforts that
could reveal gene variations responsible for a number of neurological conditions such as
autism. The work was reported in an advance, online Early Edition of the Proceedings of
the National Academy of Sciences (PNAS) the week of August 17, 2009. The research grew out
of a larger project called the Thematic Organized Psychosis (TOP) study, led by Ole
Andreassen at Ullelvål University Hospital and Institute of Psychiatry at the University
of Oslo in Norway. TOP called for using extensive magnetic resonance imaging (MRI)
scanning of hundreds of patients, including many with severe mental disorders, in
collaboration with Anders Dale of the University of California, San Diego (UCSD), School
of Medicine. Recognizing the potential of genetic studies conducted in conjunction with
the braining imaging, the team reached out to include Nicholas Schork, a genetics expert
at Scripps Research. In deciding a first target, the group decided to focus on a gene
known as MECP2 because it plays major roles in controlling brain development. Past studies
with mice have shown that MECP2 regulates the activity of a wide range of other genes
important in brain development. Substantial mutations in the gene also cause the rare
disease Retts syndrome, in which brain growth slows, leading to a range of debilitating
neurological problems and mental retardation. MECP2 has also been linked to autism.
1,4 Dioxane Found in Leading
Natural Brands
The Organic Consumers Association hosts a
press conference to announce results of a new study of natural and organic body care
products. Sadly many brands are using petroleum and contain 1,4 Dioxane a known cause of
cancer.
Ronnie Cummins: Organic vs. Natural
Organic Heroes keynote panel 7/26/09 at
Kickapoo Country Fair, La Farge, Wisc. Ronnie Cummins, director of the Organic Consumers
Association, talks about the impact of pesticides and the real difference between organic
and natural foods.
Vaccines and Childhood Illnesses:
Beyond Thimerosal. David Ayoub, MD
Presentation by David Ayoub, M.D., a
radiologist from Springfield, Illinois. From the 65th Annual Meeting of the Association of
American Physicians and Surgeons, September 12, 2008.
Mini herseninfarcten door
vaccinaties - Dr Andrew Moulden
What do we do when Medical science catches
up to public health practices? This 3 DVD series proves, in medical physiology and
clinical sciences, with new and old diagnostic technologies, that ALL vaccinations cause
immediate and delayed, acute and chronic, permanent and transient, disease and disorders
that cut across all organ systems.Tissue damages are a result of impaired blood flow and
blood 'sludging" in the microscopic vessels throughout the circulatory system.
Autism, ADHD, Sudden infant death, Gardasil, Gulf war syndrome, specific learning
disabilities, seizures and more.
Interview with Dr. Shiv Chopra
This is an interview (23 minutes) between
Dr. Shiv Chopra, a Health Canada whistleblower, with Dr. Paul Connett, Diretor of the
Fluoride Action Network. Dr. Chopra talks about his upcoming book (to be published in the
Fall, 2008) entitled "Rotten to the Core: Memoirs of a Health Canada
whistleblower." He relates his experiences to Health Canada's continued promotion of
fluoridation, despite growing evidence of harm in the scientific literature
This is an advance of a video documentary
about 7 guys searching for a meaning
Elevated arginase levels contribute
to vascular eye disease such as diabetic retinopathy
Elevated levels of the enzyme arginase contribute to vascular eye damage and Medical
College of Georgia researchers say therapies to normalize its levels could halt
progression of potentially blinding diseases such as diabetic retinopathy. Their work,
published in the August issue of The American Journal of Pathology, is the first to make
the connection between eye disease and arginase, an enzyme known to be a player in
cardiovascular disease, according to researchers at MCG and Charlie Norwood Veterans
Affairs Medical Center. "The goal is to find a new strategy for preventing
progression of diabetic retinopathy," says Dr. Ruth Caldwell, a cell biologist at the
MCG School of Medicine and VA Medical Center, and the study's corresponding author.
Because they could measure arginase levels in the blood, it also could become a biomarker
for a disease process that can work silently in the eye for months or even years, she
says. More broadly, understanding just how arginase regulates inflammation should lead to
new therapies for many acute and chronic inflammatory diseases in the eyes and other
organs, says Dr. Wenbo Zhang, postdoctoral fellow in Dr. Caldwell' lab and the paper's
first author. The researchers suspect an elevated arginase level is a red flag of early
vascular damage in the eyes as well as the heart, kidneys and other organs. "We don't
think this is going to be specific to the retina," Dr. Caldwell says, noting that
inflammation often precedes full blown vascular disease. "We know that people with
diabetes have a greater incidence of heart attack and we know that vision is a sense that
suffers greatly in diabetes," says Dr. R. William Caldwell, study co-author who
chairs the Department of Pharmacology and Toxicology in the MCG School of Medicine.
"We are finding arginase is a common player."
Study shows how to boost value of
Alzheimer's-fighting compounds
The polyphenols found in red wine are thought to help prevent Alzheimer's disease, and new
research from Purdue University and Mount Sinai School of Medicine has shown that some of
those compounds in fact reach the brain. Mario Ferruzzi, a Purdue associate professor of
food science; Connie Weaver, Purdue's head of foods and nutrition; and Elsa Janle, a
Purdue associate professor of foods and nutrition, found that the amount of polyphenols
from grapeseed extract that can reach a rat's brain is as much as 200 percent higher on
the 10th consecutive day of feeding as compared to the first. Many previous experiments,
in which absorption was measured after single or sporadic doses, often found very little,
if any, of the bioactive polyphenols reaching brain tissues. However, more chronic
exposure appears to improve absorption. "This shows that reasonable and chronic
consumption of these products may be the way to go, rather than single, high doses,
similar to drugs," said Ferruzzi, who collaborated on the research with Mount Sinai's
Dr. Giulio Pasinetti. "It's like eating an apple a day, not a case of apples over two
days every month."
MS Patients Who Smoke Show More
Brain Atrophy, More Lesions, than MS Nonsmokers
Persons with multiple sclerosis who smoked for a little as six months during their
lifetime had more destruction of brain tissue and more brain atrophy than MS patients who
never smoked, a study by neuroimaging specialists at the University at Buffalo has shown.
Research published in the Aug. 18, 2009, issue of Neurology®, the medical journal of the
American Academy of Neurology, showed that "ever-smokers" had more brain lesions
and greater loss of brain volume, as well as higher scores on the Expanded Disability
Status Scale (EDSS), than MS patients who had no history of smoking.
Research points to new target for
stopping colon cancer
Drugs that target the epidermal growth factor receptor, or EGFR, have been used for a
number of cancers. But these drugs called EGFR inhibitors, such as cetuximab, have not
been very effective against colon cancer. The new study, however, shows that drugs that
target the closely related receptor ERBB3 would probably be much more effective than EGFR
inhibitors at treating most colorectal cancers, said David Threadgill, Ph.D., adjunct
professor in the department of genetics at UNC and lead author of the study. He also is a
member of the UNC Lineberger Comprehensive Cancer Center and a professor in the genetics
department at North Carolina State University. The researchers genetically blocked ERBB3
in a mouse model of colon cancer and in human colon cancer cell lines. “If you
genetically remove ERBB3, as you would if you were pharmacologically targeting it, then
the mice rarely develop colon cancer,” Threadgill said.
NIH researchers identify key factor
that stimulates brain cancer cells to spread
Researchers funded by the National Institutes of Health have found that the activity of a
protein in brain cells helps stimulate the spread of an aggressive brain cancer called
glioblastoma multiforme (GBM). In a move toward therapy, the researchers showed that a
small designer protein can block this activity and reduce the spreading of GBM cells grown
in the laboratory. GBM is the most lethal form of brain cancer, with about half of
patients expected to die within a year of diagnosis. GBM is named for the fact that the
cancerous cells have properties of support cells in the brain called glial cells. Rather
than simply growing in a single tumor mass, GBM cells tend to migrate throughout the
brain, making it difficult to remove them surgically. As the cells spread and multiply,
they also tend to become resistant to radiation and chemotherapy. "Interventions to
control the spreading of glioblastoma multiforme have the potential to slow the clinical
course of the disease and improve overall survival rates," says Jane Fountain, Ph.D.,
a program director at NIH's National Institute of Neurological Disorders and Stroke
(NINDS). NINDS funded the new study through an initiative that encourages research on why
brain tumor cells are so highly invasive and how to therapeutically target these cells.
The study's senior author is Susann Brady-Kalnay, Ph.D., a neuroscientist at Case Western
Reserve University in Cleveland and an expert on the development of the retina. For years,
she has studied how cells migrate to their proper places in the developing retina. In
particular, she studied how this process is regulated by cell adhesion molecules –
proteins at a cell's surface that can keep the cell stuck to its surroundings, or help the
cell move. She has shown that a cell adhesion molecule called PTPmu is required for
retinal cell migration. Investigating the role of PTPmu in GBM dispersal was a logical
extension, she says. "We know that cell adhesion is important for development, and
that there are many parallels between what happens during development and what happens in
cancer," says Dr. Brady-Kalnay. For instance, she notes there is some evidence that
cancer cells have turned back the developmental clock and reverted to an embryonic stem
cell-like state.
How mercury becomes toxic in the
environment
Naturally occurring organic matter in water and sediment appears to play a key role in
helping microbes convert tiny particles of mercury in the environment into a form that is
dangerous to most living creatures. This finding is important, say Duke University
environmental engineers, because it could change the way mercury in the environment is
measured and therefore regulated. This particularly harmful form of the element, known as
methylmercury, is a potent toxin for nerve cells. When ingested by organisms, it is not
excreted and builds up in tissues or organs. In a series of laboratory experiments, Amrika
Deonarine, a graduate student in civil and environmental engineering at Duke's Pratt
School of Engineering, found that organic matter and chemical compounds containing sulfur
– known as sulfides -- can readily bind to form mercury sulfide nanoparticles. Since
they are more soluble than larger particles, these nanoparticles may be the precursors to
a process known as methylation.
Fatigue related to radiotherapy may
be caused by inflammation
Patients who experience fatigue during radiotherapy for breast or prostate cancer may be
reacting to activation of the proinflammatory cytokine network, a known inflammatory
pathway, according to a report in Clinical Cancer Research, a journal of the American
Association for Cancer Research. Julie Bower, Ph.D., an associate professor in the
Department of Psychology and Psychiatry at the University of California, Los Angeles, and
colleagues, conducted an observational study among 28 patients with breast cancer and 20
patients with prostate cancer, all early stage. Patients completed questionnaires and
provided blood samples so researchers could determine the level of proinflammatory
markers. As expected, there was a strong link between radiotherapy treatment and fatigue.
In a new finding, the researchers noted that increases in serum markers of cytokine
activity, specifically IL-1 receptor antagonist and C-reactive protein, were also linked
with fatigue. "This study suggests that exposure to radiation is releasing these
inflammatory cytokines and that may be contributing to fatigue," said Bower.
Tobacco plants yield the first
vaccine for the dreaded 'cruise ship virus'
Scientists have used a new vaccine production technology to develop a vaccine for
norovirus, a dreaded cause of diarrhea and vomiting that may be the second most common
viral infection in the United States after the flu. Sometimes called the "cruise ship
virus," this microbe can spread like wildfire through passenger liners, schools,
offices and military bases. The new vaccine is unique in its origin — it was
"manufactured" in a tobacco plant using an engineered plant virus. Researchers
are enlisting plants in the battle against norovirus, swine flu, bird flu, and other
leading infectious diseases. This plant biotechnology opens the door to more efficient,
inexpensive ways to bring vaccines quickly to the public, especially critical in times
when viruses mutate into unpredictable new strains, said Charles Arntzen, Ph.D., who
reported on the topic today at the 238th National Meeting of the American Chemical Society
(ACS). "The recent outbreak of H1N1 influenza virus has once again reminded us of the
ability of disease-causing agents to mutate into new and dangerous forms," Arntzen
points out. "It will be at least six months until a vaccine for this new strain will
be available, and it will take even longer to create large stock piles of vaccine. For a
case like the H1N1 influenza virus, you want to be able to move very rapidly and introduce
a commercial vaccine in the shortest possible time. We think we have a major advantage in
using engineered plant viruses to scale-up vaccine manufacture within weeks instead of
months."Noroviruses are always mutating, making it a moving target for vaccine
developers. Arntzen says this has presented an obstacle for big pharmaceutical companies
who might have considered developing a vaccine. Production costs can skyrocket when a
single disease may frequently require new vaccines that must be developed and tested for
safety and effectiveness. As a result, vaccines do not exist for many diseases that sicken
enormous numbers of people each year. Arntzen notes that plant biotechnology could create
a cheaper, quicker vaccine manufacturing technique uniquely suited to combat mutating
viruses like norovirus and the flu. Norovirus temporarily disables its victims, giving
them severe diarrhea or nausea for up to three days. While not as life-threatening as the
flu, Arntzen says it is equally important.
Researchers find genetic link
between physical pain and social rejection
UCLA psychologists have determined for the first time that a gene linked with physical
pain sensitivity is associated with social pain sensitivity as well. Their study indicates
that variation in the mu-opioid receptor gene (OPRM1), often associated with physical
pain, is related to how much social pain a person feels in response to social rejection.
People with a rare form of the gene are more sensitive to rejection and experience more
brain evidence of distress in response to rejection than those with the more common form.
The research was published Aug. 14 in the early online edition of Proceedings of the
National Academy of Sciences and will appear in the print version in the coming weeks. The
findings give weight to the common notion that rejection "hurts" by showing that
a gene regulating the body's most potent painkillers — mu-opioids — is involved
in socially painful experiences too, said study co-author Naomi Eisenberger, UCLA
assistant professor of psychology and director of UCLA's Social and Affective Neuroscience
Laboratory. In the study, researchers collected saliva samples from 122 participants to
assess which form of the OPRM1 gene they had and then measured sensitivity to rejection in
two ways. First, participants completed a survey that measured their self-reported
sensitivity to rejection. They were asked, for example, how much they agreed or disagreed
with statements like "I am very sensitive to any signs that a person might not want
to talk to me."
Mother's immune system may block
fetal treatments for blood diseases
Pediatric researchers have resolved an apparent contradiction in the field of prenatal
cell transplantation— a medical approach that holds future promise in correcting
sickle cell disease and other serious congenital blood disorders. In a new study in
animals, the researchers showed that the mother's immune response interferes with the
offspring's earlier ability to tolerate transplanted donor cells. The study team concludes
that focusing on transplant techniques that avoid the maternal immune response may allow
scientists to take advantage of fetal tolerance to achieve a long-sought goal of treating
blood diseases prenatally. While cautioning that much work must be done to understand how
these animal findings apply to humans, the current findings are "surprising but
reassuring," said study leader Alan W. Flake, M.D., of the Children's Center for
Clinical Research at The Children's Hospital of Philadelphia. The study appeared online
August 3 in the Journal of Clinical Investigation. For over 50 years, explained Flake, it
has been a fundamental precept of immunology that a fetus tolerates foreign antigens in a
window-of-opportunity period before its immune system fully develops the capacity to mount
an immune response. Scientists assumed that by carefully introducing donor cells and
stimulating a fetus to develop tolerance to those cells, one could set the stage for a
later organ or cellular transplant that would not be rejected by a more mature immune
system. As prenatal diagnosis has continued to become available for a greater number of
congenital diseases, scientists have considered the possibility of correcting blood
disorders such as sickle cell disease or thalassemia. After first transplanting a small
number of healthy cells in an early-stage fetus to establish tolerance, a second dose of
transplanted cells later in gestation would proliferate, and treat the blood disorder
before birth. Researchers use hematopoietic cells—stem cells that that develop into
blood cells—in this technique, in utero hematopoietic cell transplantation (IUHCT).
Antioxidants not associated with
increased melanoma risk
Antioxidant supplements do not appear to be associated with an increased risk of melanoma,
according to a report in the August issue of Archives of Dermatology, one of the
JAMA/Archives journals. A recent randomized trial of antioxidants for cancer prevention
found that daily supplementation with nutritionally appropriate doses of vitamins C and E,
beta carotene, selenium and zinc appeared to increase the risk of melanoma in women
four-fold, according to background information in the article. Because an estimated 48
percent to 55 percent of U.S. adults use vitamin or mineral supplements regularly, the
potential harmful effects of these nutrients is alarming, the authors note. Maryam M.
Asgari, M.D., M.P.H., of Kaiser Permanente Northern California, Oakland, and colleagues
examined the association between antioxidants and melanoma among 69,671 women and men who
were participating in the Vitamins and Lifestyle (VITAL) study, designed to examine
supplement use and cancer risk. At the beginning of the study, between 2000 and 2002,
participants completed a 24-page questionnaire about lifestyle factors, health history,
diet, supplement use and other cancer risk factors. Intake of multivitamins and
supplements during the previous 10 years, including selenium and beta carotene, was not
associated with melanoma risk in either women or men. The researchers also examined the
risk of melanoma associated with long-term use of supplemental beta carotene and selenium
at doses comparable to the previous study and found no association. "Consistent with
the present results, case-control studies examining serologic [blood] levels of beta
carotene, vitamin E and selenium did not find any association with subsequent risk of
melanoma," the authors write. "Moreover, the Nurses' Health Study reported no
association between intake of vitamins A, C and E and melanoma risk in 162,000 women
during more than 1.6 million person-years of follow-up."
Does sugar feed cancer?
Researchers at Huntsman Cancer Institute at the University of Utah have uncovered new
information on the notion that sugar "feeds" tumors. The findings may also have
implications for other diseases such as diabetes. The research is published in the journal
Proceedings of the National Academy of Sciences. "It's been known since 1923 that
tumor cells use a lot more glucose than normal cells. Our research helps show how this
process takes place, and how it might be stopped to control tumor growth," says Don
Ayer, Ph.D., a Huntsman Cancer Institute investigator and professor in the Department of
Oncological Sciences at the University of Utah. During both normal and cancerous cell
growth, a cellular process takes place that involves both glucose (sugar) and glutamine
(an amino acid). Glucose and glutamine are both essential for cell growth, and it was long
assumed they operated independently, but Ayer's research shows they are inter-dependent.
He discovered that by restricting glutamine availability, glucose utilization is also
stopped. "Essentially, if you don't have glutamine, the cell is short circuited due
to a lack of glucose, which halts the growth of the tumor cell" Ayer says. The
research, spearheaded by Mohan Kaadige, Ph.D., a postdoctoral fellow in Ayer's lab,
focused on MondoA, a protein that is responsible for turning genes on and off. In the
presence of glutamine, MondoA blocks the expression of a gene called TXNIP. TXNIP is
thought to be a tumor suppressor, but when it's blocked by MondoA , it allows cells to
take up glucose, which in turn drives tumor growth. Ayer's research could lead to new
drugs that would target glutamine utilization, or target MondoA or TXNIP. Ayer says the
next step in his research is to develop animal models to test his ideas about how MondoA
and TXNIP control cell growth. "If we can understand that, we can break the cycle of
glucose utilization which could be beneficial in the treatment of cancer," Ayer says.
Vitamin D Controversy and the
Marshall Protocol
This video explains the controversy
surrounding the marshall protocol as used to treat Lyme Disease and other chronic
illnesses such as sarcoidosis, fibromyalgia, etc.
UFO plus drones in Mexico
Another witness come foward
regarding a spinning UFO on MAY 22, 2009. This was near MEXICO CITY and both videos where
taken within miles away! One video is facing the sun and the other is behind the UFO.
Home
Where the hell is Matt?
The Dumbing Down of America
Retrain The Brain is a program that is
specially designed to manage and eventually elimanate ADD & ADHD, without the use of
amphetamine drugs. It also has a strong positive influence on other learning disabilities,
including autism, brain damage and dyslexia. Using only therapeutic music and handwriting
exercises, the program builds attention spans, counteracts the negative influence of TV,
takes away the risk of addiction/abuse of the amphetamine drug Ritalin and improves
penmenship.
Charlotte Iserbyt - Deliberate
Dumbing Down of the World
Charlotte Iserbyt served as Senior Policy
Advisor in the Office of Educational Research and Improvement (OERI), U.S. Department of
Education, during the first Reagan Administration, where she first blew the whistle on a
major technology initiative which would control curriculum in America's classrooms.
"Freedom is never more than one generation away from extinction. We didn't pass it to
our children in the bloodstream. It must be fought for, protected, and handed on for them
to do the same, or one day we will spend our sunset years telling our children and our
children's children what it was once like in the United States where men were free."
~Ronald Reagan, 40th president of U.S.
Dumbing Down America Mass Media
Programming
Dumbing Down Children in the Education
System and the Mass Media Programming of America. Your Government is Getting Exactly What
It's Paying For.
Hidden World: Cymatics
The work of German photographer Alexander
Lauterwasser is presented in the context of Cymatics, the study of vibration and its
effects on form-making. A brief history of Cymatic research is presented starting with the
sound-figure experiments of Ernst Chladni and Hans Jenny. Alexander Lauterwasser is shown
continuing the research that Chladni and Jenny began with his custom-built equipment that
enables him to produce beautiful geometric patterns in substances ranging from sand to
water. The connection of sound to organic patterns in nature and the philosophical
implications are also addressed.
Regarding the 7/7/2005 terrorist attacks in
London, let us look at the facts, and what we were told, and compare them. Then, using
Ockham’s Razor and common-sense, let us see what conclusions are to be drawn, so we
can all understand what most likely really did happen that day.
Tapped Trailer
Tapped is a film that examines the role of
the bottled water industry and its effects on our health, climate change, pollution, and
our reliance on oil.
Gene vital to brain's stem cells
implicated in deadly brain cancer
Researchers from Columbia University Medical Center's Herbert Irving Comprehensive Cancer
Center have identified a protein that activates brain stem cells to make new neurons
– but that may be hijacked later in life to cause brain cancer in humans. The protein
called Huwe1 normally functions to eliminate other unnecessary proteins and was found to
act as a tumor suppressor in brain cancer. These findings, published in the August 18
issue of Developmental Cell, were co-led by Antonio Iavarone, M.D., associate professor of
neurology and pathology & cell biology and Anna Lasorella, M.D., assistant professor
of pediatrics and pathology & cell biology, both of Columbia's Institute for Cancer
Genetics at the Herbert Irving Comprehensive Cancer Center. "By identifying the
normal function of Huwe1, we were able to learn that deregulation of Huwe1 function is
involved in tumor development," say Dr. Iavarone. "This demonstrates that a
gene's basic function must be understood before we can learn how it also plays a role in
the development of cancer," says Dr. Lasorella. During normal brain development,
neural stem cells grow and divide rapidly before developing into neurons. To successfully
change into neurons, they must remove all proteins that keep the cells in an immature,
stem cell state. To understand how brain tumors develop, Drs. Iavarone's and Lasorella's
teams decided that they needed to understand the development of normal neural stem cells.
Their research demonstrated that Huwe1 is responsible for "crowd control" for
the mechanism that regulates the stem cell mass in the developing brain – effectively
weeding out unnecessary stem cell-specific proteins – and promoting neurogenesis.
Without Huwe1, Dr. Lasorella discovered that in mice, too few mature neurons form in the
brain, resulting in the brain failing to properly develop. Because the stem cells and
cancer cells share the capacity for rapid proliferation, but cancer cells have lost crowd
control, Dr. Iavarone then looked for signs of Huwe1 alterations in human brain tumors.
Compared to normal brain tissue, he found that Huwe1 activity in tumors was significantly
lower than in normal brain tissue. "The loss of Huwe1 may be an important factor in
the development of brain cancer, suggesting that Huwe1 protein function may be used for
new therapeutic targets to fight deadly brain cancer," says Dr. Lasorella. "Our
next step will be to analyze the structural changes in Huwe1, and research ways to restore
this gene in brain tumor patients," says Dr. Iavarone. "In mice, giving Huwe1
back blocks the ability of normal stem cells to proliferate and develop tumors. We are
hopeful that if we can restore Huwe1 activity in brain tumor cells resulting from Huwe1
deletion, then we can stop the tumor growth."
Researchers develop new,
more-sensitive assay for detecting DNA methylation in colon cancer
A study published in this week's online issue of Nature Biotechnology, demonstrates a
unique and highly sensitive method for detecting methylation-associated cancers. Chemical
modification of DNA via the addition or deletion of methyl groups has been established as
a common biological means of activating or silencing genes. Abnormal levels of DNA
methylation, which effectively disrupt the genes responsible for normal cell cycle
regulation, has been implicated in a number of different cancers, and has led to the
development of novel cancer biomarkers. However, methylation events are rare and difficult
to detect in clinically relevant samples of blood, serum, sputum, urine or feces using
currently available methods of analysis. In a joint effort between Case Western Reserve
University and John's Hopkins University, researchers have developed a highly sensitive
method for detecting methylated DNA. The authors say the new method, known as
Methyl-BEAMing (beads, emulsion, amplification and magnetics) technology, enables absolute
quantification of the number of methylated molecules in a sample, and can detect as few as
one methylated molecule in approximately 5000 unmethylated molecules in DNA from plasma
and fecal samples, an over 60-fold improvement over an alternative commonly used detection
method. The enhanced sensitivity of the test was achieved through the use of PCR
amplification of individual DNA fragments covalently attached to specially coated magnetic
beads. The process of amplification involved suspending the magnetic beads in tiny
water-based nano-compartments immersed in droplets of oil. The beads contained a DNA
sequence specific for exon1 of the vimentin gene – a gene known to be hypermethylated
in colorectal cancer. If the vimentin gene sequence was present in the sample, subsequent
PCR resulted in thousands of copies of the gene attached to each individual magnetic bead.
Following amplification, the DNA-coated beads could be hybridized with fluorescent probes
specific to the state of methylation, sorted and analyzed using flow cytometry. The
researchers say that this method has enabled the accurate detection of a single copy of
methylated vimentin sequence in a mixture and improved the technical sensitivity for
detecting methylated vimentin exon1 by at least 62 –fold relative to standard
methylation-specific PCR. Using this novel method of digitally detecting methylated DNA,
the researchers demonstrated that the test could be used to detect 59 percent of colon
cancers in the blood, a 4-fold improvement over CEA, a serum marker commonly used to
follow colon cancer patients for recurrence of disease. Additionally, the new method could
detect 41 percent of colon cancers in the stool, as well as half of pre-cancerous polyps.
The study was led by Bert Vogelstein of John's Hopkins University and Sanford Markowitz,
M.D., Ph.D., the Markowitz-Ingalls Professor of Cancer Genetics at the Case Western
Reserve University School of Medicine and an oncologist at the Ireland Cancer Center of
University Hospitals Case Medical Center. Colon cancer is the second leading cause of
cancer death in the United States. This year 150,000 individuals will develop the disease
and 50,000 will die from it. Researchers say that deaths from colon cancer are completely
preventable when the disease is detected in its early stages, before it has spread beyond
the colon – yet many individuals do not get screened by colonoscopy.
Scientists at St. Jude Children's Research Hospital have identified inherited variations
in two genes that account for 37 percent of childhood acute lymphoblastic leukemia (ALL),
including a gene that may help predict drug response. The findings stem from the first
complete search of the human genetic blueprint or genome to look for inherited risk
factors for ALL, the most common childhood cancer. Published in the August 16 advance
online issue of Nature Genetics, the work offers the first proof based on a complete
survey of the human genome that inheritance play a role in childhood ALL.Mary Relling,
Pharm.D., St. Jude Pharmaceutical Sciences chair and the paper's senior author, estimated
that individuals who inherited variations in genes known as ARID5B or IKZF1 are almost
twice as likely to develop ALL as those without the variations. Even then, she said, the
risk remains low. ALL strikes roughly one in every 75,000 Americans. Sixty percent are
children and teenagers. "The genetic variations alone are not enough to cause the
cancer. Like all cancers, pediatric ALL is a multi-factor disease," Relling
explained. "But these findings may give us a handle on the mechanism of the disease
and drug responsiveness to it." Exactly the same genes, ARID5B and IKZF1, were
confirmed to be altered in British children with ALL. That study was published by the
Institute of Cancer Research in Surrey, England, in the same issue of Nature Genetics. In
the St. Jude study, researchers collaborated with colleagues from the Children's Oncology
Group (COG), who provided additional cases for genetic analysis. COG is an international
group of medical institutions that cooperate in research studies and clinical trials of
childhood cancer treatment. Researchers scanned the genomes of 441 children with ALL and a
control group of 17,958 cancer-free individuals for more than 300,000 common genetic
variations known as single nucleotide polymorphisms or SNPs. The search found 18 SNPs that
differed significantly in frequency between individuals with and without ALL. Six of the
18 SNPs were associated with one of the four main subtypes of ALL.
Up to 90 percent of US paper money
contains traces of cocaine
You probably have cocaine in your wallet, purse, or pocket. Sound unlikely or outrageous?
Think again! In what researchers describe as the largest, most comprehensive analysis to
date of cocaine contamination in banknotes, scientists are reporting that cocaine is
present in up to 90 percent of paper money in the United States, particularly in large
cities such as Baltimore, Boston, and Detroit. The scientists found traces of cocaine in
95 percent of the banknotes analyzed from Washington, D.C., alone. Presented here today at
the 238th National Meeting of the American Chemical Society, the new study suggests that
cocaine abuse is still widespread and may be on the rise in some areas. It could help
raise public awareness about cocaine use and lead to greater emphasis on curbing its
abuse, the researchers say. The scientists tested banknotes from more than 30 cities in
five countries, including the U.S., Canada, Brazil, China, and Japan, and found
"alarming" evidence of cocaine use in many areas. The U.S. and Canada had the
highest levels, with an average contamination rate of between 85 and 90 percent, while
China and Japan had the lowest, between 12 and 20 percent contamination. The study is the
first report about cocaine contamination in Chinese and Japanese currencies, they
say."To my surprise, we're finding more and more cocaine in banknotes," said
study leader Yuegang Zuo, Ph.D., of the University of Massachusetts in Dartmouth. Zuo says
that the high percentage of contaminated U.S. currency observed in the current study
represents nearly a 20 percent jump in comparison to a similar study he conducted two
years ago. That earlier study indicated that 67 percent of bills in the U.S. contained
traces of cocaine. "I'm not sure why we've seen this apparent increase, but it could
be related to the economic downturn, with stressed people turning to cocaine," Zuo
says. Such studies are useful, he noted, because the data can help law enforcement
agencies and forensic specialists identify patterns of drug use in a community.
New study expands the list of
hazardous chemicals in smokeless tobacco
Attention all smokeless tobacco users! It's time to banish the comforting notion that
snuff and chewing tobacco are safe because they don't burn and produce inhalable smoke
like cigarettes. A study that looked beyond the well-researched tobacco hazards,
nitrosamines and nicotine, has discovered a single pinch –– the amount in a
portion –– of smokeless tobacco exposes the user to the same amount of another
group of dangerous chemicals as the smoke of five cigarettes. The research on polycyclic
aromatic hydrocarbons (PAH) in smokeless tobacco was reported here today at the 238th
National Meeting of the American Chemical Society (ACS). It adds to existing evidence that
smokeless contains two dozen other carcinogens that cause oral and pancreatic cancers, the
scientists say. "This study once again clearly shows us that smokeless tobacco is not
safe," said Irina Stepanov, Ph.D., who led the research team. "Our finding
places snuff on the same list of major sources of exposure to polycyclic aromatic
hydrocarbons as smoking cigarettes." PAHs are widespread environmental contaminants
formed as a result of incomplete burning of wood, coal, fat in meat, and organic matter.
PAHs form, for instance, during the grilling of burgers, steaks and other meat. The
findings come in the midst of a rise in both marketing and consumption of smokeless
tobacco, which many consumers regard as less dangerous than other forms of tobacco.
Estimates suggest that sales of moist snuff in the United States have doubled since the
1980s.
'Killer spices' provide
eco-friendly pesticides for organic fruits and veggies
Mention rosemary, thyme, clove, and mint and most people think of a delicious meal. Think
bigger…acres bigger. These well-known spices are now becoming organic agriculture's
key weapons against insect pests as the industry tries to satisfy demands for fruits and
veggies among the growing portion of consumers who want food produced in more natural
ways. In a study presented here today at the American Chemical Society's 238th National
Meeting, scientists in Canada are reporting exciting new research on these so-called
"essential oil pesticides" or "killer spices." These substances
represent a relatively new class of natural insecticides that show promise as an
environmentally-friendly alternative to conventional pesticides while also posing less
risk to human and animal health, the researcher says. "We are exploring the potential
use of natural pesticides based on plant essential oils — commonly used in foods and
beverages as flavorings," says study presenter Murray Isman, Ph.D., of the University
of British Columbia. These new pesticides are generally a mixture of tiny amounts of two
to four different spices diluted in water. Some kill insects outright, while others repel
them. Over the past decade, Isman and colleagues tested many plant essential oils and
found that they have a broad range of insecticidal activity against agricultural pests.
Some spiced-based commercial products now being used by farmers have already shown success
in protecting organic strawberry, spinach, and tomato crops against destructive aphids and
mites, the researcher says. "These products expand the limited arsenal of organic
growers to combat pests," explains Isman. "They're still only a small piece of
the insecticide market, but they're growing and gaining momentum." The natural
pesticides have several advantages. Unlike conventional pesticides, these "killer
spices" do not require extensive regulatory approval and are readily available. An
additional advantage is that insects are less likely to evolve resistance — the
ability to shrug off once-effective toxins — Isman says. They're also safer for farm
workers, who are at high risk for pesticide exposure, he notes.
Protein plays unexpected role
protecting chromosome tips
A protein specialist that opens the genomic door for DNA repair and gene expression also
turns out to be a multi-tasking workhorse that protects the tips of chromosomes and
dabbles in a protein-destruction complex, a team lead by researchers at The University of
Texas M. D. Anderson Cancer Center reports in the Aug. 13 edition of Molecular Cell.
"Instead of being a really important tool dedicated just to regulation of gene
transcription, Gcn5 is more like a Swiss Army knife that performs different functions
depending on what needs to be done in the cell," said senior author Sharon Dent,
Ph.D., professor in M. D. Anderson's Department of Biochemistry and Molecular Biology. The
researchers document a chain of events that starts with depletion of Gcn5, which leads to
decreased activity by another protein that protects yet a third protein from destruction.
That last protein, TRF1, protects telomeres, dense structures at the end of chromosomes
which, like the compressed plastic tips on the ends of a shoelace, keep the chromosome
ends intact. Variation in the gene that expresses the middle protein in this model,
ubiquitin specific protease 22 (USP22), is part of an 11-gene signature associated with
highly metastatic cancers and poor prognosis, the authors note. "Our results indicate
that the Gcn5 complex regulates not just gene transcription but also protein
stability," Dent said. "They also suggest that the role of USP22 in highly
aggressive cancers might be due to these new functions."
Brain innately separates living and
non-living objects for processing
For unknown reasons, the human brain distinctly separates the handling of images of living
things from images of non-living things, processing each image type in a different area of
the brain. For years, many scientists have assumed the brain segregated visual information
in this manner to optimize processing the images themselves, but new research shows that
even in people who have been blind since birth the brain still separates the concepts of
living and non-living objects. The research, published in today's issue of Neuron, implies
that the brain categorizes objects based on the different types of subsequent
consideration they demand—such as whether an object is edible, or is a landmark on
the way home, or is a predator to run from. They are not categorized entirely by their
appearance. "If both sighted people and people with blindness process the same ideas
in the same parts of the brain, then it follows that visual experience is not necessary in
order for those aspects of brain organization to develop," says Bradford Mahon,
postdoctoral fellow in the Department of Brain and Cognitive Sciences at the University of
Rochester, and lead author of the study. "We think this means significant parts of
the brain are innately structured around a few domains of knowledge that were critical in
humans' evolutionary history." Previous studies have shown that the sight of certain
objects, such as a table or mountain, activate regions of the brain other than does the
sight of living objects, such as an animal or face—but why the brain would choose to
process these two categories differently has remained a mystery, says Mahon. Since the
regions were known to activate when the objects were seen, scientists wondered if
something about the visual appearance of the objects determined how the brain would
process them. For instance, says Mahon, most living things have curved forms, and so many
scientists thought the brain prefers to processes images of living things in an area that
is optimized for curved forms. To see if the appearance of objects is indeed key to how
the brain conducts its processing, Mahon and his team, led by Alfonso Caramazza, director
of the Cognitive Neuropsychology Laboratory at Harvard University, asked people who have
been blind since birth to think about certain living and non-living objects. These people
had no visual experience at all, so their brains necessarily determined where to do the
processing using some criteria other than an object's appearance.
Obesity increases risk of prostate
cancer recurrence for both blacks and whites
A new look at a large database of prostate cancer patients shows that obesity plays no
favorites when it comes to increasing the risk of recurrence after surgery: Being way
overweight is equally bad for blacks and whites, say researchers at Duke University
Medical Center. Studies have shown that obesity is linked to generally worse outcomes in
many cancers, including prostate cancer. Because blacks are more likely than whites to
develop and die from prostate cancer – and because there is a higher prevalence of
obesity among black men with prostate cancer, compared to whites – some studies have
suggested that obesity might be a more ominous risk factor for blacks than whites.
"Not so," says Stephen Freedland, M.D., an associate professor of urology and
pathology in the Duke Prostate Center and the senior author of the study appearing in the
journal Cancer. "Obesity leads to worse cancer in both groups." Freedland and
Jayakrishnan Jayachandran, M.D. a urologic oncology fellow at Duke and the lead author of
the paper, examined the records of 1,415 men enrolled in the Shared Equal Access Regional
Cancer Hospital (SEARCH) database who had undergone a radical prostatectomy. Black men
comprised almost half (47 percent) of the sample. After adjusting for various preoperative
characteristics, researchers analyzed the relationship between body mass index (BMI) and
the aggressiveness of the cancer, as measured by the risk of recurrence. In contrast to
other studies, investigators found no association between race and obesity. Almost a third
of the men were obese, regardless of race. "We found that higher BMI was associated
with significantly increased risk of cancer recurrence for both blacks and whites,"
said Jayachandran. "Though prior SEARCH-based studies from our group found that
obesity was associated with a higher risk of disease progression as measured by a rising
PSA after surgery, it now appears that being obese just means a poorer prognosis, period,
regardless of race." As for why that might be, Jayachandran says he's not sure, but
he says it may have something to do with altered hormone levels.
Scarring key to link between
obesity and diabetes
The team, in collaboration with University Hospital Aintree, the University of Warwick and
researchers in Sweden, found that people classified as obese and those with pre-diabetes
have raised levels of a protein called SPARC, that can cause tissue scarring. The research
revealed that an increase in insulin, a hormone that controls blood sugar levels, and
leptin, a hormone that regulates appetite, can trigger an increase in SPARC, which can
prevent the proper storage of fat in fat tissue cells. It is thought that leptin, in an
attempt to balance energy levels in the body, could trigger SPARC to limit the storage of
fat. SPARC can do this by increasing the formation of scars in fat tissue, which can
prevent fat being stored safely in the body. Researchers found that this process could
predispose obese patients to type 2 diabetes. Professor John Wilding, from the
University's School of Clinical Science, explains: "We tested fat tissue of patients
at University Hospital Aintree and found that an increase in leptin also increases SPARC
levels, which reduces the safe storage of fat through the development of abnormal tissue
scarring. Scarring of fat tissue is known to increase as we gain weight and we found that
this is exacerbated by leptin, as well as an increase in insulin, produced by the
pancreas." Dr Katarina Kos, lead author of the research, added: "Leptin is
produced in fat cells to regulate appetite, but the body becomes resistant to the effects
of appetite reduction in obese patients. Leptin continues to increase in response to
overall fat mass and promotes scarring through increased SPARC levels. Once scarring
occurs, the excess nutritional energy from fat cannot be taken up by fat cells and so
remains in the blood and begins to gather around organs. As a result, fat cells of people
classified as obese, may not fulfil their natural purpose to store fat." Diabetes is
caused by the cells' inability to respond to insulin, which would normally enable uptake
of sugar from the blood. To compensate, the pancreas creates more insulin to clear blood
sugar from the circulation. The pancreas becomes exhausted and is unable to produce
sufficient insulin to keep up with the demands of the body. This results in the
development of type 2 diabetes, which can cause problems such as lack of energy to the
cells and, over time, damage to the eyes, kidneys and heart. The research team, working
with the Swedish fast food study group at Linkoping University, also found that weight
gain, induced by more than doubling calorie intake through eating 'junk food', causes
SPARC levels to increase by 33%. In a further study with the University of Gothenburg,
scientists found that a reduced calorie diet can decrease SPARC levels and the stimulus
for tissue scarring. Researchers are now investigating why some people are more prone to
fat tissue scarring than others and how further understanding of SPARC could contribute to
future treatments for diabetes.
MRC scientists advance
understanding of cell death
Medical Research Council (MRC) scientists have made an important advance in understanding
the biological processes involved when cells are prompted to die. The work may help
scientists to eventually develop new treatments for the many common diseases and
conditions which occur when cell death goes wrong. The research, published in leading
journal Molecular Cell [1] today (Friday 14 August 2009) was carried out by a team of
scientists, at the MRC Toxicology Unit at the University of Leicester and a subsequent
patent application has been filed by MRC Technology, the commercial arm of the MRC. cells
in the human body are continually dying and most of these cells kill themselves by a form
of cell death, commonly referred to as apoptosis. In a healthy body, the number of cells
stays constant. Millions of new cells are produced every second, and millions of others
are lost or kill themselves. Failure of the normal apoptosis process plays a role in
different diseases including cancer, certain neurodegenerative disorders such as
Parkinson's and immune diseases, such as autoimmune lymphoproliferative syndrome (ALPS).
One of the study's authors, Dr Marion MacFarlane, MRC Toxicology Unit, explained:
"This new research takes us a step closer to understanding how the DISC triggers
cells to die. The challenge now is to try and use this fundamental knowledge to help work
towards finding better treatments for conditions which occur when DISC-mediated cell death
goes wrong." Previous research has shown that a complex called the 'DISC', which is
made up of different proteins and is formed following activation of molecules called
'Death Receptors', can trigger apoptosis by 'switching on' key players in the cell death
process. However, previous research has found that the DISC can also activate cell
survival, thus raising the question as to how paradoxically the 'DISC' can trigger these
opposing cellular outcomes? Now, scientists at the MRC Toxicology Unit have found that the
DISC can trigger cell death or cell survival by switching the activity of key
death-promoting molecules. Stopping the 'DISC' from functioning properly prevents the cell
death programme from being carried out efficiently and instead results in cell survival.
Thus, in diseases such as ALPS, where a crucial death-promoting protein is often not
active the DISC fails to function properly.
New study suggests possible genetic
links between environmental toxins and multiple myeloma
The International Myeloma Foundation (IMF)—supporting research and providing
education, advocacy and support for myeloma patients, families, researchers and
physicians—today said newly published data may provide a possible genetic link
between environmental toxins and bone disease in multiple myeloma. Myeloma, also called
multiple myeloma, is a cancer of cells in the bone marrow that affect production of blood
cells and can damage bone. Once considered a "rare disease of the elderly," it
is increasingly being diagnosed in patients under 45 years old, including some of the
early responders to the 9/11 World Trade Center site. Now a study published this week may
help explain why. The study from researchers with the IMF gene bank, Bank on a Cure®,
identified several changes in DNA sequences called SNPs (single nucleotide polymorphisms)
that are associated with a risk of bone disease in myeloma. Further analyses showed that
many of these DNA changes may be involved with the way the human body responds to certain
environmental toxins, providing a possible link between myeloma and the environment. The
findings were published in the latest issue of the journal Leukemia*. Brian G.M. Durie,
M.D., lead author of the study and Chairman of the IMF said: "This is a
hypothesis-generating study. While the functional role of many SNPs is still uncertain,
this study is supportive of the notion that genetic factors affecting toxin breakdown may
be related to the development of myeloma. This gives us an important starting point for
further studies." The findings may help explain a widely reported study this week in
the Journal of Occupational and Environmental Medicine, that found more cases of myeloma
among younger responders to the 9/11 World Trade Center site than would normally be
expected. The findings are also supportive of a study published earlier this year that
suggests a link between certain pesticide exposures in agricultural workers and a
precursor to multiple myeloma. Previous studies have also shown an increased risk for
myeloma among firefighters, and the IMF has issued guidelines for firefighters for the
prevention and treatment of this disease. "Multiple myeloma is not a familiar cancer
to patients or even to many doctors, but taken together, these studies say it should not
be overlooked," said Susie Novis, President and Co-founder of the IMF. "While
multiple myeloma cannot be cured, it can be treated with new, targeted therapies including
REVLIMID®, VELCADE® and THALOMID®. These studies tell us it is critically important for
medical practitioners to know the possible risk factors for myeloma along with the early
warning signs so they will be alerted to test for it." Myeloma affects an estimated
750,000 people worldwide, and in industrialized countries it is being diagnosed in growing
numbers and in increasingly younger people.
First compound that specifically
kills cancer stem cells found
The cancer stem cells that drive tumor growth and resist chemotherapies and radiation
treatments that kill other cancer cells aren't invincible after all. Researchers reporting
online on August 13th in the journal Cell, a Cell Press publication, have discovered the
first compound that targets those cancer stem cells directly. "It wasn't clear it
would be possible to find compounds that selectively kill cancer stem cells," said
Piyush Gupta of the Massachusetts Institute of Technology (MIT) and the Broad Institute.
"We've shown it can be done." The team including MIT's Robert Weinberg and the
Broad Institute's Eric Lander developed a new high-throughput screening method that makes
it possible for the first time to systematically look for agents that kill cancer stem
cells. That ability had previously eluded researchers due to the rarity of those cells
within tumor cell populations and their relative instability in laboratory culture. In the
new study, the researchers manipulated cultured breast cancer cells to greatly enrich for
those with the stem-like properties, including increased resistance to standard cancer
drugs. They then screened a library of 16,000 natural and commercial chemical compounds
for their ability to kill those stem-like cells and not other cancer cells. That screen
turned up 32 contenders. The researchers narrowed that list down to a handful of chemicals
that they could readily get in sufficient quantities for further testing on normal cancer
stem cells. Of those, one called salinomycin was the clear winner. Salinomycin reduced the
proportion of breast cancer stem cells by more than 100-fold compared to a commonly used
chemotherapeutic drug for breast cancer called paclitaxel (aka Taxol™).
Salinomycin-treated cells were less able than paclitaxel-treated ones to seed tumors when
injected into mice, they report. Salinomycin treatment also slowed the growth of the
animals' tumors.
New method takes aim at aggressive
cancer cells
A multi-institutional team of Boston-area researchers has discovered a chemical that works
in mice to kill the rare but aggressive cells within breast cancers that have the ability
to seed new tumors. These cells, known as cancer stem cells, are thought to enable cancers
to spread — and to reemerge after seemingly successful treatment. Although further
work is needed to determine whether this specific chemical holds therapeutic promise for
humans, the study shows that it is possible to find chemicals that selectively kill cancer
stem cells. The scientists' findings appear in the August 13 advance online issue of Cell.
"Evidence is accumulating rapidly that cancer stem cells are responsible for the
aggressive powers of many tumors," says Robert Weinberg, a Member of Whitehead
Institute for Biomedical Research and one of the authors of the study. "The ability
to generate such cells in the laboratory, together with the powerful techniques available
at the Broad Institute, made it possible to identify this chemical. There surely will be
dozens of others with similar properties found over the next several
years.""Many therapies kill the bulk of a tumor only to see it regrow,"
says Eric Lander, Director of the Broad Institute of MIT and Harvard, and an author of the
Cell paper. "This raises the prospect of new kinds of anti-cancer therapies." An
emerging idea in cancer biology is that tumors (breast, prostate, colon, lung, etc.)
harbor a group of cells with the unique ability to regenerate cancers. In addition to
promoting tumor growth, these so-called cancer stem cells are largely resistant to current
cancer therapies. If it were possible to identify chemicals that selectively kill cancer
stem cells, such chemicals might become critical candidates for future drug development.
However, researchers have struggled to study cancer stem cells directly in the laboratory.
The cells' relative scarcity compared to other tumor cells, combined with a tendency to
lose their stem cell-like properties when grown outside of the body, have severely limited
the amount of material available for analysis.
An apple a day keeps kidney stones
away
Researchers have found another reason to eat well: a healthy diet helps prevent kidney
stones. Loading up on fruits, vegetables, nuts, low-fat dairy products, and whole grains,
while limiting salt, red and processed meats, and sweetened beverages is an effective way
to ward off kidney stones, according to a study appearing in an upcoming issue of the
Journal of the American Society Nephrology (JASN). Because kidney stones are linked to
higher rates of hypertension, diabetes, increased body weight, and other risk factors for
heart disease, the findings have considerable health implications. Eric Taylor, MD (Maine
Medical Center) and his colleagues at Brigham and Women's Hospital conducted a large study
to determine the effects of healthy eating habits on the formation of kidney stones. The
investigators collected information from individuals enrolled in three clinical studies:
the Health Professionals Follow-up Study (45,821 men followed for 18 years), the Nurses'
Health Study I (94,108 older women followed for 18 years), and the Nurses' Health Study II
(101,837 younger women followed for 14 years). Dr. Taylor's team assigned a score to each
participant based on eight components of a DASH (Dietary Approaches to Stop Hypertension)
style diet: high intake of fruits, vegetables, nuts and legumes, low-fat dairy products,
and whole grains and low intake of salt, sweetened beverages, and red and processed meats.
Individuals with higher DASH scores consumed diets that were higher in calcium, potassium,
magnesium, oxalate, and vitamin C and lower in sodium. A total of 5,645 incident kidney
stones developed in the participants in the three studies. In each study, participants
with the highest DASH scores were between 40% and 45% less likely to develop kidney stones
than participants with the lowest DASH scores. The reductions in kidney stone risk were
independent of age, body size, fluid intake, and other factors. Because a DASH-style diet
may affect the development of hypertension, diabetes, and other chronic diseases
associated with kidney stones, the researchers also performed an analysis limited to study
participants without hypertension or diabetes. Even among those individuals the DASH diet
reduced the risk of kidney stones. Many of the medications used to treat kidney stones
have unpleasant side effects. This study indicates that adopting a DASH-style diet may be
an effective alternative.
Carnegie Mellon develops innovative
method to detect genetic causes of complex diseases
Computational biologists at Carnegie Mellon University have developed an analytical
technique to detect the multiple genetic variations that contribute to complex disease
syndromes such as diabetes, asthma and cancer, which are characterized by multiple
clinical and molecular traits. Rather than searching one at a time for genetic alterations
that cause a particular symptom or trait, as in most conventional approaches, the Carnegie
Mellon scientists use a statistical method that enables them to uncover genome variations
underlying an entire regulatory network of genes or traits that are responsible for
complex diseases. Professor Eric P. Xing and postdoctoral scientist Seyoung Kim report
today in the online journal Public Library of Science (PLoS) Genetics that their
graph-guided fused lasso (GFlasso) method showed increased power in detecting gene
variants associated with complex symptoms compared with other methods. In one test,
GFlasso successfully detected a gene variant already implicated in severe asthma and
identified two additional variants that had not previously been associated with the
condition. More study of the two variants will be necessary to confirm the association,
Xing and Kim said. "We know that some of the most common and most serious diseases
that plague humans are caused not by a single genetic mutation, but by a combination of
many genetic and environmental factors," said Xing, an associate professor of machine
learning, language technologies and computer science. "Complicating the situation is
that most complex diseases have a large number of clinical traits such as various
symptoms, body metrics and family history, and that genome-wide gene expression profiling
can identify tens of thousands of molecular traits associated with the disease."
Novel Treatment Reduces Swollen
Livers
A novel treatment strategy for patients with many cysts in their liver led to a surprising
result, reported in the online version of Gastroenterology by researchers from Radboud
University Nijmegen Medical Centre, The Netherlands. A six month treatment with a
synthetic gastrointestinal hormone lanreotide significantly decreased swollen cystic
livers by approximately five percent, compared to a ‘wait and see’ policy. At
least five percent of the population has one or two cysts in the liver. Cysts are
fluid-filled cavities. There are also many patients who have numerous cysts, which then is
termed a polycystic liver. These cysts cause the liver to grow to four to six times its
normal size. Until recently, surgery was the only possible treatment for these patients,
but this approach leads to many complications, and the outcome is not always successful.
Ultimately, these patients need a liver transplantation, but in view of the limited
availability of organs, only few are actually transplanted.
Bad news for coffee drinkers who
get headaches
People who consume high amounts of caffeine each day are more likely to suffer occasional
headaches than those with low caffeine consumption, a team of researchers at the Norwegian
University of Science and Technology (NTNU) reports in a study recently published in the
Journal of Headache Pain. But in findings that had “no obvious reason”, the
researchers, led by Knut Hagen from NTNU’s Faculty of Medicine, also reported that
low caffeine consumption was associated with a greater likelihood of chronic headaches,
defined as headaches for 14 or more days each month. The results are drawn from a large
cross-sectional study of 50,483 people who answered a questionnaire about caffeine
consumption and headache prevalence as a part of the Nord-Trøndelag Health Survey (HUNT
2), a county-wide health survey conducted in 1995-1997 on a wide range of health topics.
Obstructive sleep apnea is
prevalent in adults with Down syndrome
A study in the Aug. 15 issue of the Journal of Clinical Sleep Medicine shows that adults
with Down syndrome also frequently suffer from obstructive sleep apnea (OSA). However,
complications of untreated OSA such as cardiovascular disease, daytime sleepiness and
impaired cognitive functioning overlap with the manifestations of Down syndrome;
therefore, OSA may not be detected. Results indicate that 94 percent of subjects with Down
syndrome had OSA; 88 percent had at least moderate OSA with an apnea-hypopnea index (AHI)
of more than 15 breathing pauses per hour of sleep; and 69 percent had severe OSA with an
AHI of more than 30. Twelve of the 16 subjects with Down syndrome were obese, and there
was a significant correlation between body mass index (BMI) and AHI. Total sleep time in
subjects with Down syndrome (307 minutes) was more than an hour less than in controls (380
minutes). Despite the severity of OSA in the study group, medical evaluation had been
sought in only one case. According to senior author Carole Marcus, M.B.B.Ch., professor of
pediatrics at the University of Pennsylvania and director of the Children's Hospital of
Philadelphia Sleep Center, it is well known that children with Down syndrome are at risk
for OSA, with a prevalence of 30 to 55 percent, and adults with Down syndrome have even
more predisposing factors for OSA than children, as they still have the craniofacial
anomalies and are more likely to be obese or hypothyroid. "Patients with Down
syndrome have a great deal of risk factors for OSA (based on their narrow midface, large
tongue, floppy muscle tone, tendency towards being overweight, and thyroid disease),"
said Marcus. "However, the fact that almost all of the subjects studied had OSA was a
much higher prevalence than we expected. It was surprising how severe the illness was, and
how the OSA was unsuspected by their caregivers."
Cognitive Behavioral Therapy for
Insomnia Improves Sleep and Pain in People with Osteoarthritis
A study in the Aug. 15 issue of the Journal of Clinical Sleep Medicine shows that the use
of cognitive behavioral therapy for insomnia (CBT-I) is an effective treatment for older
patients with osteoarthritis and comorbid insomnia.Results show that treatment improved
both immediate and long-term self-reported sleep and pain in older patients with
osteoarthritis and comorbid insomnia without directly addressing pain control.
Participants who received CBT-I reported significantly decreased sleep latency (by an
average of 16.9 minutes initially, and by 11 minutes a year after treatment) and wake
after sleep onset (by an average of 37 minutes initially, and by 19.9 minutes a year after
treatment), significantly reduced pain (by 9.7 points initially, and by 4.7 points a year
after treatment) and increased sleep efficiency (by 13 percent initially, and by 8 percent
a year after treatment). These improvements persisted in CBT-I patients (19 of 23) who
were further assessed for sleep quality and perceived pain at a one-year follow-up visit.
According to lead author Michael V. Vitiello, PhD, professor at the University of
Washington in Seattle, Wash., results indicate that insomnia is not merely a symptom of
osteoarthritis but rather a co-existing illness. Vitiello said improving sleep can result
in an improvement in osteoarthritis, which is particularly important because, at least in
older adults, insomnia rarely exits by itself; rather it typically coexists with other
illnesses, pain conditions and depression. “The particular strength of CBT-I is that
once an individual learns how to improve their sleep, study after study has shown that the
improvement persists for a year or more,” said Vitiello. “What we and others are
showing is that CBT-I can not only improve sleep but that improvement of sleep may lead to
improvement in co-existing medical or psychiatric illnesses, such as osteoarthritis or
depression, and in the case of our study, that these additional benefits can be seen in
the long term.” A total of 23 patients with a mean age of 69 years were randomly
assigned to CBT-I, while 28 patients with a mean age of 66.5 years were assigned to a
stress management and wellness control group. Participants in the control group reported
no significant improvements in any measure.
USC researchers identify
'regulatory' genetic sequences that may predict risk for prostate cancer
Researchers at the Keck School of Medicine of the University of Southern California (USC)
have identified a novel genetic mechanism that may govern an individual's risk of
developing prostate cancer. The findings, published today in the Public Library of Science
(PLoS) Genetics journal, found mechanisms involved in cancer-associated sites in areas
where no genes are present (gene 'deserts') at a chromosomal region called 8q24. The new
findings show that some of these sites have embedded regulatory sequences that act as
enhancers of gene expression, modulated by genetic variation, or single nucleotide
polymorphisms (SNPs). The two-year study, conducted by researchers from USC, Harvard
University and the Weizmann Institute of Tel Aviv, Israel, found novel functions of SNPs
in areas where no genes were present. They found how the SNPs are able to modulate genetic
expression even while they were near no genes. SNPs denote a modest increase in risk for
certain diseases; in this particular chromosomal area, the SNPs appear to be influencing
gene expression for prostate (and other) cancer 'at a genetic distance'. "The real
contribution of this discovery is that we get a feel for a previously unappreciated
mechanism that may be a predisposition to this disease," said Gerhard (Gerry)
Coetzee, Ph.D., professor of urology and preventive medicine at the Keck School of
Medicine and principal investigator on the study. "We have unearthed a new way to
understand the risk for prostate cancer." The study was prompted by discrepancies in
prostate cancer risk among ethnic groups. Currently, risk factors for prostate cancer are
governed by age, and a disproportionate increased risk chiefly among African-American men,
with Caucasian men following and Asian men last. This gene 'desert' featuring versions of
particular SNPs are found more often in African-American men and may explain their
increased risk for the disease.
