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Week 34
Educate yourself to boost
achievement in kids
With school days just around the corner, a University of Michigan researcher has some
advice for parents who want to increase their children's academic success. "If you
want your kids to do well in school, then the amount of education you get yourself is
important," said Pamela Davis-Kean, a psychologist at the U-M Institute for Social
Research (ISR). "This may mean that parents need to go back to school. "A
growing number of large-scale, long-term studies now show that increasing parental
education beyond high school is strongly linked to increasing language ability in
children. Even after controlling for parental income, marital status and a host of other
factors, we find that the impact of parental education remains significant."
Live recordings of cell
communication
A new advanced method for nano-scale imaging of vesicle-fusion – vesicles are
biological nano-sized containers - could add to our understanding of diseases of the
nervous system and viral infections. In the long term, this could be useful in developing
a cure for neurological diseases and mental disorders (e.g. schizophrenia, depression,
Parkinson's disease, Alzheimer's disease). Researchers from the Department of Neuroscience
and Pharmacology and the Nano-Science Center at the University of Copenhagen are behind
the new data, which have recently been published in the prestigious scientific journal
PNAS. Neurons communicate with each other with the help of nano-sized vesicles. Disruption
of this communication process is responsible for many diseases and mental disorders like
e.g. depression. Nerve signals travel from one neuron to another through vesicles - a
nano-sized container loaded with neurotransmitter molecules. A vesicle fuses with the
membrane surrounding a neuron, releases neurotransmitters into the surroundings that are
detected by the next neuron in line. However, we still lack a more detailed understanding
of how the fusion of vesicles occurs on the nano-scale.
'Green' energy from algae
In view of the shortage of petrochemical resources and climate change, development of
CO2-neutral sustainable fuels is one of the most urgent challenges of our times. Energy
plants like rape or oil palm are being discussed fervently, as they may also be used for
food production. Hence, cultivation of microalgae may contribute decisively to tomorrow's
energy supply. For energy production from microalgae, KIT scientists are developing closed
photo-bioreactors and novel cell disruption methods. Microalgae are monocellular,
plant-like organisms engaged in photosynthesis and converting carbon dioxide (CO2) into
biomass. From this biomass, both potential resources and active substances as well as
fuels like biodiesel may be produced. While growing, algae take up the amount of CO2 that
is later released again when they are used for energy production. Hence, energy from algae
can be produced in a CO2-neutral manner contrary to conventional energy carriers. Apart
from CO2-neutral closed loop management, algae have an-other advantage: Industrial CO2
emissions may be used as a "re-source", as algae grow faster at high carbon
dioxide concentrations and, hence, produce more biomass for energy production. However,
this is not their only advantage: "Compared to land plants, algae produce five times
as much biomass per hectare and contain 30 to 40% oil usable for energy production",
says Professor Cle-mens Posten, who directs this research activity at the KIT Institute of
Life Science Engineering. As the algae may also be cultivated in arid i.e. dry, areas not
suited for agriculture, there is hardly any competition with agricultural areas. There,
however, closed systems are required.
Beep, beep, oops, what was I doing?
"That blasted siren. I can't focus." That reaction to undesired distraction may
signal a person's low working-memory capacity, according to a new study. Based on a study
of 84 students divided into four separate experiments, University of Oregon researchers
found that students with high memory storage capacity were clearly better able to ignore
distractions and stay focused on their assigned tasks. Principal investigator Edward K.
Vogel, a UO professor of psychology, compares working memory to a computer's random-access
memory (RAM) rather than the hard drive's size -- the higher the RAM, the better
processing abilities. With more RAM, he said, students were better able to ignore
distractions. This notion surfaced in a 2005 paper in Nature by Vogel and colleagues in
the Oregon Visual Working Memory & Attention Lab. In experiments with some variations
in approaches -- detailed in the July 8 issue of the Journal of Neuroscience -- students'
brain activity was monitored using electroencephalography (EEG) while they studied images
on a computer screen, recognizing a shape with a missing component, and then identifying
the object after it moved simply to another location or amid distractions. Using a
"task irrelevant probe" -- a 50 millisecond-long flash of light -- Vogel and
Keisuke Fukuda, a doctoral student of Vogel's and lead author, were able to determine
where exactly a subject's attention was focused. All of the subjects were able to quickly
and accurately identify the targets when the objects moved around the screen, but as
distracting components were added some maintained accuracy while others diverted their
attention and slipped in performing the assigned tasks. (Vogel describes his research in a
video at: http://www.youtube.com/watch?v=cmToeopS9bY.) Vogel is quick to say that the
findings don't necessarily signify problems for an easily distracted person, although
people who hold their focus more intensely tend to have higher fluid intelligence; they
score higher on achievement tests, do better in math and learn second languages easier
than peers who are captured by interruptions. Vogel currently is working with other UO
researchers to explore if the easily distracted indeed have a positive side, such as in
artistic creativity and imagination. The new research, funded by the National Science
Foundation, zeroed in on the brain's prefrontal cortex -- a region linked to executive
function and under scrutiny for its association with many neurological disorders -- and
the intraparietal sulcus (IPS), which is involved in perceptual-motor coordination,
including eye movements.
First human gets new antibody aimed
at hepatitis C virus
Building upon a series of successful preclinical studies, researchers at MassBiologics of
the University of Massachusetts Medical School (UMMS) today announced the beginning of a
Phase 1 clinical trial, testing the safety and activity of a human monoclonal antibody
they developed that can neutralize the Hepatitis C virus (HCV). The first volunteer
received the antibody known as MBL-HCV1 on July 28, 2009, and the study is now proceeding
and will eventually involve 30 healthy subjects in a dose-escalation trial expected to
conclude later this year. "We are pleased that this program has now entered the
clinical trial phase," said Donna Ambrosino, MD, executive director of MassBiologics
and a professor of pediatrics at the Medical School. "This trial will test the safety
of the antibody and measure its activity in the subjects. This will help us determine the
useful dose and other parameters as we plan for the next step in this program, which will
be a Phase 2 study in liver transplant patients." HCV attacks the liver and can
eventually lead to liver failure. According to the U.S. Centers for Disease Control and
Prevention, 3.2 million Americans are chronically infected with HCV and some 10,000 die
annually of the disease. Globally, as many as 170 million people are estimated to suffer
from HCV infection. For the most serious cases of HCV that do not respond to antiviral
drugs, liver transplantation is the only option. HCV is the leading indication for liver
transplantation, diagnosed in about half of the 6,000 liver transplants done each year in
the United States. Transplantation can be a life-saving treatment; however, in nearly all
cases the patient's new liver is eventually infected by HCV because the virus remains in
the patient's bloodstream during surgery. The powerful antiviral drugs now used to attack
HCV prior to end-stage liver failure are not routinely used during surgery due to the
patients' weakened condition and because of the strong medication that must be used to
prevent the body from rejecting the new liver. After re-infection with HCV, nearly 40
percent of patients suffer rapid liver failure, with markedly reduced survival rates.
New cancer drug delivery system is
effective and reversible
For cancer drug developers, finding an agent that kills tumor cells is only part of the
equation. The drug must also spare healthy cells, and – ideally – its effects
will be reversible, to cut short any potentially dangerous side effects.University of
Illinois researchers report that they have assembled a new cancer drug delivery system
that, in cell culture, achieves all of the above. The findings appear this month in the
journal Angewandte Chemie. The team began with the knowledge that small, membrane-bound
compartments, called liposomes, are useful as drug-delivery vehicles. When linked to
molecules that target receptors on cancer cells, liposomes can enter and dump their
cancer-killing contents into those cells. Scientists have spent more than a decade trying
to direct liposomes to specific cancer cells, with limited success. A common approach
involves attaching an antibody to the liposome membrane. Ideally the antibody will bind to
a cancer cell receptor so that it can deliver the liposome – and the cancer drug
– into the cell. Developing such antibodies is costly and time-consuming, however,
and the process of attaching them to liposomes is difficult to control. Antibodies spur an
immune response, requiring extra steps to create a useable therapeutic agent, and the
ability of antibody-conjugated liposomes to bind to cancer cells can be inconsistent. Some
small molecules, such folate, a vitamin, also work as cancer cell targeting agents, but
those now in use are not as good as antibodies at binding to cancer cells. To solve the
cell-targeting problem, the U. of I. team turned its attention to small molecules called
aptamers.
Unstable proteins can cause
premature ageing
The normal ageing process has long been linked to problems with cell respiration, the
process through which the cells extract energy from nutrients. Researchers at the Swedish
medical university Karolinska Institutet have now shown how certain proteins that are
synthesised in the cellular mitochondria – popularly known as the cells' power plants
– become unstable and disintegrate, which in turn can impair cell respiration and
cause premature ageing. Every time we inhale, the blood transports the oxygen from our
lungs to our cells' mitochondria, where it is used to convert the nutrients in our food
into a form of energy that the body can use. Problems with this process, called cell
respiration, have been linked to numerous conditions, from rare genetic diseases to
diabetes, cancer, Parkinson's disease and the normal ageing process. For cell respiration
to function properly, it needs proteins synthesised outside and then imported into the
mitochondria, and proteins synthesised within the mitochondria themselves from their own
DNA (mtDNA). It has long been known that an accumulation of harmful mutations of mtDNA can
cause premature ageing, but just how this happens has remained something of a mystery.
Scientists at Karolinska Institutet in Stockholm have now shown through studies on mice
that changes in mtDNA can cause ageing by introducing errors into the proteins
manufactured by the mitochondria. The amount of protein is normal, but the proteins are
rendered unstable and quickly disintegrate, leading eventually to the breakdown of cell
respiration. "Our results show that premature ageing is caused by point mutations in
the mtDNA, which cause the mitochondrial proteins to become unstable and
disintegrate," says Aleksandra Trifunovic, one of the scientists involved in the
study.
Yale researchers find key to
keeping cells in shape
Yale University researchers have discovered how a protein within most cell membranes helps
maintain normal cell size, a breakthrough in basic biology that has implications for a
variety of diseases such as sickle cell anemia and disorders of the nervous system. Cell
size is regulated by the balance of positively and negatively charged ions and other
solutes in the fluid inside and outside cells, which in turn prevents water from moving
across cell membranes and changing cell size. Changes in chemical composition of
extracellular fluid can disrupt this balance, sometimes with damaging consequences to
health. "If you eat a bag of salty potato chips or a jug of water, the cells lining
your stomach will be under pressure to shrink or expand," explains Richard Lifton,
senior author of the paper and Sterling Professor of Genetics and Internal Medicine.
"Cells need to rapidly change their ionic composition to compensate and avoid blowing
up like balloons or shrinking like raisins, and they do this by almost instantly changing
their chloride levels." In the Aug. 7 issue of the journal Cell, a team of Yale
scientists led by Jesse Rinehart, associate research scientist in genetics and Lifton, an
investigator of the Howard Hughes Medical Institute, report they used innovative new
quantitative proteomics technologies to identify two key regulatory transporter sites that
control the exit of potassium and chloride out of cells. The proteomics technologies allow
scientists to observe specific sites on proteins that undergo phosphorylation.
Phosphorylation is a common and reversible modification made to a protein after it is
synthesized and can turn a protein's function on or off. The Yale scientists show that the
regulatory sites they identified are almost completely phosphorylated under normal
conditions, when the transporter is inactive. When confronted with changes in the
environment that challenge the cell, the proteins are rapidly dephosphorylated and
dramatically increase transport activity. "These transporters are overactive in
sickle cell anemia and play a role in the dehydration of sickle cells," said Patrick
Gallagher, professor of pediatrics at the Yale School of Medicine and a co-author of the
study. "With this new information, we may be able to find new strategies to
manipulate this activity and identify new treatments that are so urgently needed."
Gallagher's lab is already studying genetic variations in the potassium-chloride pathway
in a search of new drug targets.
Women often opt to surgically
remove their breasts, ovaries to reduce cancer risk
Many women at high risk for breast or ovarian cancer are choosing to undergo surgery as a
precautionary measure to decrease their cancer risk, according to a report in Cancer
Epidemiology, Biomarkers & Prevention, a journal of the American Association for
Cancer Research. "Women have their breasts or ovaries removed based on their risk. It
does not always happen immediately after counseling or a genetic test result and can take
more than seven years for patients to decide to go forward with surgery," said lead
researcher D. Gareth Evans, M.D. Evans is a consultant in clinical genetics at the Genesis
Prevention Center, University Hospital of South Manchester NHS Trust and a professor at
the University of Manchester, United Kingdom. Evans and colleagues assessed the increase
in risk-reduction surgery among women with breast cancer and evaluated the impact of
cancer risk, timing and age. Rate of increase was measured among 211 women with known
unaffected BRCA1 or BRCA2 mutation carriers. BRCA1 and BRCA2 are hereditary gene mutations
that indicate an increased risk for developing breast cancer. Additionally, more than
3,500 women at greater than 25 percent lifetime risk of breast cancer without mutations
also had a documented increase in risk-reduction surgery. Women who had a biopsy after
undergoing risk evaluation were twice as likely to choose a risk-reducing mastectomy.
Forty percent of the women who were mutation carriers underwent bilateral risk-reducing
mastectomy; 45 percent had bilateral risk-reducing salpingo-oophorectomy (surgical removal
of ovaries). These surgeries are widely used by carriers of BRCA1 and BRCA2 gene mutations
to reduce the risk for breast and ovarian cancer. Evaluated by gene type, bilateral
risk-reducing salpingo-oophorectomy was more common in women who were BRCA1 gene carriers
— 52 percent had the surgery compared with 28 percent of the women who were BRCA2
gene carriers. "We found that older women were much less likely to have a mastectomy,
but were more likely to have their ovaries removed," said Evans.
Stanford scientists find common
trigger in cancer and normal stem cell reproduction
Researchers at Stanford University School of Medicine have discovered, for the first time,
a common molecular pathway that is used by both normal stem cells and cancer stem cells
when they reproduce themselves.In a paper to be published Aug. 7 in the journal Cell,
Michael Clarke, MD, the Karel H. and Avice N. Beekhuis Professor in Cancer Biology, and
his colleagues showed that breast cancer stem cells and normal breast stem cells turn down
the creation of a specific group of cell signals when they are reproducing. Increasing the
amount of one of these signals, called miR-200c, strongly suppressed the ability of both
cancer stem cells and normal stem cells to divide and reproduce. The discovery of a common
regulatory pathway in both kinds of stem cells supports the idea that cancer stem cells
and normal stem cells share fundamental properties. "This very strongly supports the
cancer stem cell hypothesis," said Clarke, who is associate director of the Stanford
Stem Cell Biology and Regenerative Medicine Institute and a member of the Stanford Cancer
Center. "A lot of people have speculated that there was this molecular link between
these two kinds of cells (cancer stem cells and normal stem cells), but this is the first
time we have actually identified it." The cancer stem cell hypothesis states that
cancers are a collection of many different kinds of cells, only a very few of which create
and sustain the cancer. These are the cancer stem cells, which share many traits with
normal stem cells. While most cells in the body cannot reproduce themselves, stem cells
have the ability to do so, and can also create the cells that mature into various tissues.
Blood stem cells, for instance, which reside in the bone marrow, have the ability to
create new blood stem cells and also to create all the different types of mature blood
cells. While the current discovery is important evidence of how cancer stem cells operate,
it does not automatically lead to new cancer therapies. "The problem is that if we
attack cancer using this mechanism, it is also going to affect normal stem cells which are
essential for our survival," Clarke said. But understanding how cancer cells sustain
themselves may in the future offer new ways of attacking the disease. "The hope is
that we can find nuances that distinguish between how normal stem cells renew themselves
and how cancer stem cells do so, and then use those differences to attack only the
cancer," said Clarke.
Iron-binding drug could help
diabetics heal stubborn wounds, says Stanford/Einstein study
A drug used to remove iron from the body could help doctors fight one of diabetes’
cruelest complications: poor wound healing, which can lead to amputation of patients’
toes, feet and even legs. The drug, deferoxamine, helped diabetic mice heal small cuts 10
days faster than those who did not receive treatment, according to researchers from
Stanford University School of Medicine and the Albert Einstein College of Medicine. The
team is now working to arrange human trials for deferoxamine. If the results translate, it
could help doctors combat such diabetic complications as foot ulcers, an “unmet
medical need of gigantic proportions,” said Geoffrey Gurtner, MD, professor of
surgery and senior author on the paper published July 27 in the Proceedings of the
National Academy of Science.
Psychologists offer ways to improve
prison environment, reduce violent crime
U.S. prisons are too punitive and often fail to rehabilitate, but targeting prisoners'
behavior, reducing prison populations and offering job skills could reduce prisoner
aggression and prevent recidivism, a researcher told the American Psychological
Association on Saturday. "The current design of prison systems don't work," said
criminal justice expert Joel Dvoskin, PhD, of the University of Arizona. "Overly
punitive approaches used on violent, angry criminals only provide a breeding ground for
more anger and more violence." Presenting at the American Psychological Association's
117th Annual Convention, Dvoskin discussed his upcoming book, "Applying Social
Science to Reduce Violent Offending," which examines why prisons are failing and what
needs to change. "Prison environments are replete with aggressive behaviors, and
people learn from watching others acting aggressively to get what they want," Dvoskin
said in an interview. Applying behavior modification and social learning principles can
work in corrections, he said. "For example, systematic reinforcement of pro-social
behaviors is a powerful and effective way to change behavior, but it has never been used
as a cornerstone of corrections," he said. Also, punishment can be effective in
changing behavior, but it only works in the short term and immediately after the unwanted
behavior happens, he said. While there is a place for punishment, it should be used in
psychologically informed and effective ways. However, punishment should not be
one-size-fits-all, Dvoskin said. "We need to know what may be behind the criminal
behavior to know what the best treatment is," he said. "A person who commits
crimes when drunk but not when sober is likely suffering from an alcohol problem. Treating
the alcohol problem may diminish the criminal behavior."
Jesus gave us the name of the
Antichrist
Sugar: The Bitter Truth
The Obama Deception HQ Full length
version
The Obama Deception is a hard-hitting film that completely destroys the myth that
Barack Obama is working for the best interests of the American people. The Obama
phenomenon is a hoax carefully crafted by the captains of the New World Order. He is being
pushed as savior in an attempt to con the American people into accepting global slavery.
We have reached a critical juncture in the New World Order's plans. It's not about Left or
Right: it's about a One World Government. The international banks plan to loot the people
of the United States and turn them into slaves on a Global Plantation. Covered in
this film: who Obama works for, what lies he has told, and his real agenda. If you want to
know the facts and cut through all the hype, this is the film for you.
Deze complete film is door 2.988.791 mensen bekeken
Spectacular scenes from the Ilulissat ice fjord and the Greenland ice cap. These images
were filmed during the 2006 Climate Change College, during which 6 students from the UK
and the Netherlands ventured into the arctic wilderness to be trained as climate change
ambassadors. Based on the experiences and knowledge gathered on several locations in
Greenland, they launched various initiatives raising public awareness around the topic of
climate change.
Tuvalu - Islands on the frontline
of Climate Change
With photography by Robin Hammond of Panos Pictures, this multimedia piece looks at the
island nation of Tuvalu, as the Tuvaluan people become some of the first environmental
refugees, a direct result of man-made climate change.
The Arctic is not just raw and hostile but can also be, at times, peaceful and quiet.
Sit back, relax, and enjoy the view! This footage was recorded by Philip de Roo, Joep
Bovens, and Eric Schlameisen during their 2300km south-north crossing of the Greenland ice
cap in May/June 2008.
Belfast: Us And Them - Ireland
Kilometres of graffiti-daubed concrete walls snake through Belfast. They divide
Catholic neighbourhoods from Protestant. But do these Peace Walls keep the hatred and
suspicion locked outside or inside? The consensus among the locals is clear if the walls
came down there would be a return to intractable sectarian violence. If you pull that wall
down therell be murder, mayhem, therell be blood spilt, says a loyalist resident. The
recent killings of two soldiers, a policeman and a Catholic community worker, indicate
that trouble is still very close to the surface. Theres walls of prejudice; walls that
were built here 300 years ago and they're still here in legislation, in prejudice and
bigotry', tells Republican Sean McVeigh. 'So those are the walls that are going to have to
come down first. Are the Peace Walls monuments to the past or vital and necessary
peacekeepers in the present?
Parents can help stop the obesity
epidemic, says psychologist
Childhood obesity has quadrupled in the last 40 years, which may mean today's children
become the first generation to have a shorter lifespan than their parents, a leading
obesity expert told the American Psychological Association on Saturday. However, parents
can help stave off this impending crisis if they help their children to eat better and
exercise, according to Edward Abramson, PhD. Abramson, professor emeritus at California
State University-Chico, teaches psychology and is author of the books "Body
Intelligence" and "Emotional Eating." In the last decade, "we've seen
a [tenfold] increase in Type-2 diabetes and psychological and social consequences, such as
prejudice, rejection, discrimination and low self-esteem in children," Abramson said
at APA's 117th Annual Convention. "More than 60 percent of overweight children have
one risk factor for cardiovascular disease and 20 percent have two or more risk
factors." Bad eating habits can start with "emotional eating," or eating
when one is not hungry, or from following a strict diet, Abramson said. "This can
lead to a weight problem or an eating disorder," he added. "Parents' attitudes
and behaviors also have an influence on children's eating, and mothers more than fathers
affect children's eating habits and body image." Many factors contribute to mothers'
concern about their children's risk for obesity, Abramson said. "For example, there
is evidence that minority parents (e.g., African-American, Hispanic) are less concerned
about their children's weight," he said. "Often, when a mother is struggling
with her own weight, she becomes more involved in regulating her daughter's eating. In
general, mothers are more concerned than fathers about their child's weight, especially
their daughter's, and are more likely to restrict foods."
Conaway Lab uncovers function of
potential cancer-causing gene product
The Stowers Institute's Conaway Lab has uncovered a previously unknown function of a gene
product called Amplified in Liver Cancer 1 (Alc1), which may play a role in the onset of
cancer. The work was published yesterday by the Proceedings of the National Academy of
Science Early Edition. "We've been able to demonstrate that the protein encoded by
the Alc1 gene is, in fact, a chromatin remodeling enzyme," explained Aaron
Gottschalk, lead author on the paper and a University of Kansas Medical Center graduate
student conducting research in the Conaway Lab. "By itself, this enzyme is inactive,
but in the presence of a compound called NAD and another enzyme called poly (ADP-ribose)
polymerase 1 (Parp1), its ability to move nucleosomes on DNA is strongly activated."
Parp1 uses NAD to build a polymeric molecule, poly(ADP-ribose), that is coupled to Parp1
itself or to other proteins. The team established that binding of a specific Alc1 region
to poly(ADP-ribose) coupled to Parp1 helps recruit Alc1 to bind to and remodel nucleosomes
."This finding is particularly interesting because Parp1 and poly(ADP-ribose) are
known to play important roles in transcriptional regulation, DNA repair, and DNA
replication, but how they do so is really not at all clear," said Ron Conaway, Ph.D.,
Investigator and co-senior author on the publication. "Finding that Parp1 and
poly(ADP-ribose) recruit the chromatin remodeling enzyme Alc1 to chromatin and activate
Alc1 activity suggests a mechanism by which they might function."
Study finds no link between
cognitive decline, socioeconomic status in elderly
New UCLA research suggests that for seniors age 70 and older, socioeconomic status does
not play a major role in the brain's continued ability to function. However, seniors who
have never been married and widowers seem to perform more poorly as they age. Previous
studies on age-related cognitive decline have not adequately clarified the role
demographics and socioeconomic status might play in the rate of decline. Some small and
short-term studies have found small socioeconomic differences in decline rates, while
others have shown none at all, leaving the issue murky at best. In a new national study of
older Americans 70-plus years of age (mean age 75) published in the Aug. 1 issue of the
American Journal of Epidemiology, researchers from the David Geffen School of Medicine at
UCLA and the UCLA School of Public Health found that rates of cognitive decline over a
nine-year period were similar across socioeconomic and racial and ethnic groups. The
findings indicate that disparities in cognitive functioning among older Americans of
different groups are almost entirely due to differences in the cognitive peaks they
reached earlier in life, not to differences in rates of decline.
Fumbled handoffs can lead to
medical errors
Poor communication of the outcomes of medical tests whose results are pending at the time
of a patient's hospital discharge is common and can lead to serious medical errors in
post-hospitalization medical treatment. A new study by researchers from the Regenstrief
Institute and the Indiana University School of Medicine has found that hospital discharge
summaries are grossly inadequate at documenting both tests with pending results and
information about which doctors should receive the post-discharge test results. The
findings appear in the September 2009 issue of the Journal of General Internal Medicine.
During a hospital stay tests are ordered by emergency department physicians, generalists,
specialists, hospitalists and other medical staff. Test results such as those indicating
positive blood culture, uncontrolled thyroid or declining kidney function can require
post-discharge treatment but results of some tests may not be ready for weeks after the
patient leaves the hospital. Most patients are unaware that test results are pending.
Carbon Nanoparticles Toxic to Adult
Fruit Flies But Benign to Young
Carbon nanoparticles are widely used in medicine, electronics, optics, materials science
and architecture, but their health and environmental impact is not fully understood. The
scientists found that larval Drosophila melanogaster showed no physical or reproductive
effects from consuming carbon nanoparticles in their food. Yet adult Drosophila
experienced a different fate. Tests showed adults immersed in tiny pits containing two
varieties of carbon nanoparticles died within hours. Analyses of the dead flies revealed
the carbon nanoparticles stuck to their bodies, covered their breathing holes, and coated
their compound eyes. Scientists are unsure whether any of these afflictions led directly
to the flies’ death.
Delays in UK child brain tumour
diagnosis
Significant numbers of children in the UK are suffering from preventable levels of
disability, particularly blindness, and premature death because of poor diagnosis of brain
tumours. A new study by scientists at The University of Nottingham's Children's Brain
Tumour Research Centre, funded by the Samantha Dickson Brain Tumour Trust, shows that
prolonged and slow diagnosis can make long term survivors of childhood brain tumours up to
10 times more likely to suffer disability. 450 children in the UK are diagnosed with a
brain tumour every year. The average time between the onset of symptoms and diagnosis in
children in the UK is between two and three months, that’s up to three times longer
than the rest of Europe and the USA. David Walker, Professor of Paediatric Oncology at the
Children’s Brain Tumour Research Centre, University of Nottingham, said: “Our
study showed that the UK health system is the slowest system for making this diagnosis
compared to reports from other countries. It takes more than 13 weeks in the UK to make
this diagnosis for half of the patients, whilst in the US and Poland this is achieved
within 5 weeks. The research also showed that symptoms increased in number and that
disability increased in severity as time passed before diagnosis. This indicates that
delays in diagnosis are affecting the severity of disability for the children and young
people, which can have life-long consequences. ”
Colon Cancer May Yield to Cellular
Sugar Starvation
Scientists at the Johns Hopkins Kimmel Cancer Center have discovered how two
cancer-promoting genes enhance a tumor’s capacity to grow and survive under
conditions where normal cells die. The knowledge, they say, may offer new treatments that
starve cancer cells of a key nutrient - sugar. However, the scientists caution that
research does not suggest that altering dietary sugar will make any difference in the
growth and development of cancer. “Cancer cells adapt to living within the inner
layers of a tumor, a place where circulating nutrients are relatively scarce,” says
Nickolas Papadopoulos, Ph.D., associate professor at the Johns Hopkins Kimmel Cancer
Center. “We wanted to know what makes these cancer cells survive under such
conditions.”
The hepatitis healing power of
blueberry leaves
A chemical found in blueberry leaves has shown a strong effect in blocking the replication
of the Hepatitis C virus, opening up a new avenue for treating chronic HCV infections,
which affect 200 million people worldwide and can eventually lead to cirrhosis and liver
cancer. Among the areas of especially high Hepatitis C incidence is the Miyazaki
prefecture of southern Japan, a trend that led Hiroaki Kataoka and colleagues at the
University of Miyazaki and elsewhere in Japan on a search for better treatment options.
Currently, there is no vaccine for HCV, and though a combination drug regimen can clear
HCV infection, this treatment is only about 60% effective on average and poses risks of
severe side effects. Kataoka and colleagues believed that since HCV is localized in the
liver and can take 20 years or more to develop into disease, a dietary supplement might
help slow or stop disease progression. So they screened nearly 300 different agricultural
products for potential compounds that suppress HCV replication and uncovered a strong
candidate in the leaves of rabbit-eye blueberry (native to the southeastern US). They
purified the compound and identified it as proanthocyandin (a polyphenol similar to the
beneficial chemicals found in grapes and wine). While proanthocyandin can be harmful,
Kataoka and colleagues noted its effective concentration against HCV was 100 times less
than the toxic threshold, and similar chemicals are found in many edible plants,
suggesting it should be safe as a dietary supplement. In the meantime, the researchers now
hope to explore the detailed mechanisms of how this chemical stops HCV replication.
Narcissistic bosses destroy morale,
drive down bottom line
In recent years, the motivations of business leaders such as financier Bernard Madoff and
former Enron CEO Ken Lay have come under increased scrutiny as a result of behavior that
caused both their employees and the public considerable distress. Unquestionably, many of
the documented lapses in judgment can be traced to selfishness and a failure to check
one's ego. To better establish the level of self-serving behavior, a recent study was
conducted to examine the narcissistic tendencies of bosses in American organizations.
Wayne Hochwarter, the Jim Moran Professor of Management in the Florida State University
College of Business, asked more than 1,200 employees to provide opinions regarding the
narcissistic tendencies of their immediate supervisor. T
Bladder cells feel stretch
Japanese research group led by Prof. Makoto Tominaga and Dr. Takaaki Sokabe (National
Institute for Physiological Sciences: NIPS), and Prof. Masayuki Takeda, Dr. Isao Araki and
Dr. Tsutomu Mochizuki (Yamanashi Univ.), found that bladder urothelial cells have a sensor
for stretch stimulation. Their finding was reported in the Journal of Biological Chemistry
published on Aug 7, 2009. Bladder is known to release ATP that activates micturition
reflex pathway during urine storage. However, it has been unknown how urothelial cells
sense bladder distension. The research group examined the function of 'TRPV4' protein
abundantly expressed in urothelial cells. The group developed a special apparatus to
measure cell responses upon stretch stimulation, which mimics bladder distension. Upon
stretch stimulation, robust Ca2+ influx and following ATP release were observed in
urothelial cells. These phenomena were almost completely attributed to TRPV4 activation,
since such responses were eliminated by a TRPV4 inhibitor and reduced in TRPV4-deficient
urothelial cells. Dr. Sokabe said, "This is the first report to show that TRPV4 is a
primal stretch-detector in urothelial cells. Given that TRPV4 is critically involved in
the sensing mechanism in the bladder, development of chemicals modulating TRPV4 activity
may be useful for treatment of bladder disorders such as overactive bladder and
pollakiuria."
2 lines account for most human
embryonic stem cell research, Stanford scholar finds
For the past eight years, scientists who wanted to use federal funds for research on human
embryonic stem cells had to restrict their studies to 21 cell lines approved by the
National Institutes of Health. But an analysis by a researcher at the Stanford University
School of Medicine suggests that only two of those lines have been used routinely. "I
was surprised by these results," said Christopher Scott, director of Stanford's
Program on Stem Cells in Society. "I never imagined that we would find that
three-fourths of the requests would be for the same two cell lines." On the one hand,
the findings raise concerns about the reauthorization process of cell lines under way at
the NIH — if these lines are now excluded from federal funding due to ethical
considerations, researchers may abandon them, and their previous research, in favor of
other lines. On the other, the findings draw attention to the possibility that these two
lines may have abnormalities or characteristics that make them not as useful as newer
lines. "Not only are scientists asking for these lines, they are publishing on
them," said Scott, a senior research scholar at Stanford's Center for Biomedical
Ethics. "They have become the reference standards against which new embryonic and iPS
cell lines are being compared." (An iPS cell is an adult cell that has been induced
to look and act like a human embryonic stem cell; comparing them with existing embryonic
stem cell lines is important, as there is much debate about whether these iPS cells are
functionally equivalent to human embryonic stem cells.) Scott collaborated with
researchers from the Mayo Clinic and the University of Michigan to conduct the research,
which will be published Aug. 7 in Nature Biotechnology. Together they analyzed the number
and timing of requests placed by scientists for human embryonic stem cell lines housed at
the two largest stem cell banks in the country: the National Stem Cell Bank at the WiCell
Research Institute in Madison, Wisc., and the Harvard Stem Cell Institute in
Massachusetts. Although the National Stem Cell Bank is meant to be the source of all
NIH-approved lines, Scott and his colleagues found that at no time have all 21 lines been
available for distribution; a maximum of 18 lines were available at the beginning of this
year. Two cell lines, known as H1 and H9, made up the majority of requests — 941 out
of 1,217, or 77 percent, since 1999. One other line, H7, was requested 111 times. In
contrast, 13 of the previously approved lines were requested fewer than 10 times in the
past decade.
Teaching resilience, sense of
purpose in schools can prevent depression and improve grades
Teaching children how to be more resilient along with regular classroom instruction can
improve children's outlook on life, curb depression and boost grades, according to a
researcher who spoke at the American Psychological Association's convention Saturday.
"In the last 50 years, the U.S. population has seen an increase in their standard of
living, such as having more money, owning more homes and cars and living longer. But our
sense of meaning, purpose and satisfaction with life have not gone up, they have gone
down," said psychologist Martin Seligman, PhD, of the University of Pennsylvania.
"This has been especially detrimental to children. Nearly 20 percent of young people
experience depression." The effects can carry over to adulthood and cause early
death, more health problems, less satisfaction with jobs and relationships and higher
rates of depression, he added. Speaking at the APA's 117th annual convention, Seligman
showed how teaching resilience, positive emotion, and a sense of purpose in school can
protect children against depression, increase their life satisfaction and improve their
learning power. The researchers looked at two evidence-based programs, the Penn Resiliency
Program (PRP) and the Positive Psychology Program (PPP). The PRP sought to increase
students' ability to handle day-to-day stressors and problems that are common for
adolescents. This program was designed to prevent depression. The PRP promotes optimism by
teaching students to think more realistically and flexibly about the problems they
encounter. PRP also teaches assertiveness, creative brainstorming, decision-making,
relaxation and other coping and problem-solving skills. Seligman and his co-authors
reviewed 19 studies from the past 20 years that used PRP. These included more than 2,000
8- to 15-year-olds. All the studies used adolescents from different racial and ethnic
backgrounds and community settings. The group leaders who taught the skill were all from
professional backgrounds.
Psychological factors help explain
slow reaction to global warming, says APA task force
While most Americans think climate change is an important issue, they don't see it as an
immediate threat, so getting people to "go green" requires policymakers,
scientists and marketers to look at psychological barriers to change and what leads people
to action, according to a task force of the American Psychological Association. Scientific
evidence shows the main influences of climate change are behavioral – population
growth and energy consumption. "What is unique about current global climate change is
the role of human behavior," said task force chair Janet Swim, PhD, of Pennsylvania
State University. "We must look at the reasons people are not acting in order to
understand how to get people to act." APA's Task Force on the Interface Between
Psychology and Global Climate Change examined decades of psychological research and
practice that have been specifically applied and tested in the arena of climate change,
such as environmental and conservation psychology and research on natural and
technological disasters. The task force presented its findings at APA's 117th Annual
Convention in Toronto in a report that was accepted by the association's governing Council
of Representatives.
Climate caused biodiversity booms
and busts in ancient plants and mammals
A period of global warming from 53 million to 47 million years ago strongly influenced
plants and animals, spurring a biodiversity boom in western North America, researchers
from three research museums report in a paper published online this week in the
Proceedings of the National Academy of Sciences. "Today, the middle of Wyoming is a
vast desert, and a few antelope and deer are all you see," said lead author Michael
Woodburne, honorary curator of geology at the Museum of Northern Arizona. "But 50
million years ago, when temperatures were at their highest, that area was a tropical
rainforest teeming with lemur-like primates, small dawn horses and a number of small
forest rodents and other mammals. In fact, there were more species of mammals living in
the western part of North America at that time than at any other time." Woodburne and
co-authors Gregg Gunnell of the University of Michigan Museum of Paleontology and Richard
Stucky of the Denver Museum of Nature & Science examined the records of ancient
temperatures and information on the fossil plants and mammals that inhabited North America
during the Eocene epoch and found that diversity increased and declined with rising and
falling temperatures.
UCI discovers new Alzheimer's gene
A UC Irvine study has found that a gene called TOMM40 appears twice as often in people
with Alzheimer's disease than in those without it. Alzheimer's, for which there is no
cure, is the leading cause of elderly dementia. Having the harmful form of TOMM40
significantly increases one's susceptibility when other risk factors – such as having
a gene called ApoE-4 – are present, the new study reports. People who have ApoE-4 are
three to eight times more likely to develop Alzheimer's. "The TOMM40 gene influences
the ease with which molecules can get in and out of mitochondria, the energy production
center and stress mediator of cells. TOMM40 also processes materials that form amyloid
plaque, a hallmark of Alzheimer's," said Dr. Steven Potkin, lead author of the study
and UCI psychiatry & human behavior professor. "With aging, the number and
function of mitochondria decrease, accompanied by a parallel increased risk of developing
Alzheimer's," he said. "This study points to the use of mitochondrial-based
therapies for treating the disease."
Psychologists say longer lives can
still lead to happier golden years
As more people live well into their 80s and 90s, it's reassuring to know that most people
get happier as they age and exert more emotional control than younger adults, according to
researchers who spoke at the 117th Annual Convention of the American Psychological
Association. "Life expectancy changed because people changed the way they
lived," said Lauren Carstensen, PhD. "Now that we're here, we have to keep
adapting. We are in the middle of a second revolution and it's up to us to make adulthood
itself longer and healthier." Carstensen, a psychology professor at Stanford
University and founding director of the Stanford Center on Longevity, said the percentage
of people on the planet who are over 65 is expected to more than double by the year 2050,
and the fastest-growing segment of the population is people over age 85. Susan Turk
Charles, PhD, of the University of California, Irvine, presented a review of several
psychological studies on aging and mental health. She found that except for people with
dementia-related diseases, mental health generally improves with age. One study she cited
– a 23-year longitudinal study looking at three groups of people, each at different
stages in their lives – found that emotional happiness improved with age.
Noninsulin-producing alpha cells in
the pancreas can be converted to insulin-producing beta cells
In findings that add to the prospects of regenerating insulin-producing cells in people
with type 1 diabetes, researchers in Europe -- co-funded by the Juvenile Diabetes Research
Foundation -- have shown that insulin-producing beta cells can be derived from
non-insulin-producing cells in the pancreas. In results of a study published today in the
journal Cell, the researchers, led by Patrick Collombat of the Max-Planck Institute for
Biophysical Chemistry in Germany and Ahmed Mansouri of the University of Göttingen in
Germany, in collaboration with researchers at the JDRF Center for Beta Cell Therapy in
Diabetes in Brussels, discovered in mice that new insulin-producing beta cells can be
generated from alpha cells in the islets of the pancreas by modifying the expression of a
specific gene (Pax4) in alpha cells. (Alpha cells generate the hormone glucagon in
response to low blood sugar to restore normal blood sugar levels.) They also discovered
that the alpha cells that give rise to new beta cells originate from progenitor cells in
the pancreas. The newly formed beta cells result in better glucose control and prolonged
survival of younger mice with diabetes. In type 1 diabetes, the immune system attacks beta
cells, stopping a person's pancreas from producing insulin, the hormone that enables
people to get energy from glucose. One pathway towards a cure for type 1 diabetes may be
to restore insulin production through regeneration of insulin-producing beta cells within
a person's body, an alternative to transplanting functional beta cells from a donor.
"This study suggests that regenerating beta cells may be a viable pathway towards
restoring beta cell function in type 1 diabetes," said Richard Insel, M.D., Executive
Vice President of Research of JDRF. "It reinforces the concept that there are
progenitor cells in the mouse pancreas that can generate new beta cells under special
circumstances. And it points to some potential cellular targets for beta cell regenerative
therapeutics - both the pancreatic progenitor cells and the alpha cells. Further, the
research identifies a critical protein and pathways that can be used to screen for small
molecule drugs for developing beta cell regenerative therapeutics that target these
cells." By forcing expression in the pancreatic alpha cells of the protein Pax4 - a
so-called transcription factor capable of modifying expression of multiple genes to
regulate patterns of development or other key cellular functions - the researchers drove
the conversion of alpha cells into insulin-producing beta cells in mice. The resulting
reduction of alpha cells triggered the activation and differentiation of progenitor cells
to replace the alpha cells that had switched to beta cells.
Tumor mutations can predict chemo
success
New work by MIT cancer biologists shows that the interplay between two key genes that are
often defective in tumors determines how cancer cells respond to chemotherapy. The
findings should have an immediate impact on cancer treatment, say Michael Hemann and
Michael Yaffe, the two MIT biology professors who led the study. The work could help
doctors predict what types of chemotherapy will be effective in a particular tumor, which
would help tailor treatments to each patient. "This isn't something that's going to
take five years to do," says Yaffe, who, along with Hemann is a member of the David
H. Koch Institute for Integrative Cancer Research at MIT. "You could begin doing this
tomorrow." The work could also guide the development of new chemotherapy drugs
targeted to tumors with specific genetic mutations. Hemann, Yaffe, and their colleagues
report their results in the Aug. 15 issue of the journal Genes and Development. Koch
Institute postdoctoral associates Hai Jiang and H. Christian Reinhardt are lead authors of
the study, which the researchers say is one of the first examples of how genetic profiling
of tumors can translate to improvements in patient treatment. "There's a huge amount
of genetic information available, but it hasn't made its way into clinical practice
yet," says Hemann.
What makes stem cells tick?
Investigators at the Burnham Institute for Medical Research (Burnham) and The Scripps
Research Institute (TSRI) have made the first comparative, large-scale phosphoproteomic
analysis of human embryonic stem cells (hESCs) and their differentiated derivatives. The
data may help stem cell researchers understand the mechanisms that determine whether stem
cells divide or differentiate, what types of cells they become and how to control those
complex mechanisms to facilitate development of new therapies. The study was published in
the August 6 issue of the journal Cell Stem Cell. Protein phosphorylation, the biochemical
process that modifies protein activities by adding a phosphate molecule, is central to
cell signaling. Using sophisticated phosphoproteomic analyses, the team of Sheng Ding,
Ph.D., associate professor at TSRI, Evan Y. Snyder, M.D., Ph.D., professor and director of
Burnham's Stem Cell and Regenerative Biology program, and Laurence M. Brill, Ph.D., senior
scientist at Burnham's Proteomics Facility, catalogued 2,546 phosphorylation sites on
1,602 phosphoproteins. Prior to this research, protein phosphorylation in hESCs was poorly
understood. Identification of these phosphorylation sites provides insights into known and
novel hESC signaling pathways and highlights signaling mechanisms that influence
self-renewal and differentiation. "This research will be a big boost for stem cell
scientists," said Dr. Brill. "The protein phosphorylation sites identified in
this study are freely available to the broader research community, and researchers can use
these data to study the cells in greater depth and determine how phosphorylation events
determine a cell's fate."
Researchers uncover potential
mechanisms to protect against genetic alterations, diseases
Peering into the DNA of tiny yeast, researchers at the Moores Cancer Center at the
University of California, San Diego and the San Diego Branch of the Ludwig Institute for
Cancer Research have pinpointed a large number of genes that can prevent a type of genetic
rearrangement that may lead to cancer and other diseases. The presence of these genes and
their accompanying pathways, many of which are involved in repairing mistakes in DNA
replication, may help explain how the body fends off so many potentially damaging genetic
alterations while maintaining its stability. "We've begun to identify the pathways
that are very specific for preventing those types of rearrangements that involve DNA with
duplications," said Richard Kolodner, PhD, professor of medicine and cellular and
molecular medicine at the UC San Diego School of Medicine and the Moores UCSD Cancer
Center, and a member of the San Diego Branch of the Ludwig Institute for Cancer Research
(LICR). Reporting online in advance of publication in the August 20, 2009 issue of the
journal Nature, Kolodner and his team focused on a particular type of genetic change
called a Gross Chromosomal Rearrangement (GCR), a large-scale change in the structures of
chromosomes, which house genes. Such changes might entail a sequence of genes being
deleted or genetic material exchanging positions on chromosomes. According to Kolodner,
while the human genome contains many regions where rearrangements, genetic duplications
and other aberrations are more likely to occur – increasing the likelihood for
chromosomal mistakes and genetic mutations – the genome is surprisingly stable. To
try to better understand why, the researchers examined GCR formation in chromosome regions
in yeast (Saccharomyces cerevisiae). Using a modified version of a previously developed
test, they compared the rate and features of GCR formation in a chromosome region lacking
"at-risk" DNA sequences with that of a region containing DNA duplications, which
are more likely to drive rearrangements. These latter regions were much more like human
chromosomes. More importantly, they also looked at the effects of various genes and
pathways on the development of GCRs. The research team found that many genes and genetic
pathways that failed to block GCR formation in "lower-risk" regions actually
played a large role in suppressing GCRs in "at-risk" areas.
Extinction Runs in the Family
Global calamities like the one that doomed most dinosaurs forever alter the varieties of
life found on Earth. But new research shows that it doesn’t take a catastrophe to end
entire lineages. An analysis of 200 million years of history for marine clams found that
vulnerability to extinction runs in evolutionary families, even when the losses result
from ongoing, background rates of extinction. ”Biologists have long suspected that
the evolutionary history of species and lineages play a big role in determining their
vulnerability to extinction, with some branches of the tree of life being more
extinction-prone than others,” said Kaustuv Roy, a biology professor at the
University of California, San Diego, noting that human activities threaten some
evolutionary lineages of living vertebrates more than others. “Now we know that such
differential loss is not restricted to extinctions driven by us but is a general feature
of the extinction process itself.”
Hopkins scientists find cells
responsible for bladder cancer's spread
Johns Hopkins scientists have tracked down a powerful set of cells in bladder tumors that
seem to be primarily responsible for the cancer's growth and spread using a technique that
takes advantage of similarities between tumor and organ growth. The findings, reported in
the July Stem Cells, could help scientists develop new ways of finding and attacking
similar cells in other types of cancer. Researchers have long suspected that a subset of
cells in cancerous tumors act much like developmentally primitive cells known as stem
cells, which spur organ development early in life and remain present in nearly all the
body's organs to repair or replace injured and aging tissues. These cancer cells and stem
cells share a variety of characteristics including an unlimited lifespan and a propensity
to migrate through tissues. These same properties are the ones that make cancer
particularly dangerous, says David Berman, M.D., Ph.D., associate professor of pathology,
oncology, and urology at the Johns Hopkins University School of Medicine. If researchers
had a way to identify and specifically target cancer cells with these properties, they
could wipe out the population that sustains tumors and makes them grow. Other researchers
have identified proteins on the surfaces of these cancer cells that could work as markers,
but because other cells sometimes shared these proteins, this approach can lead to errors,
Berman says.
Hundreds of New Species Discovered
in Fragile Eastern Himalayas
Over 350 new species including the world’s smallest deer, a “flying frog”
and a 100 million-year old gecko have been discovered in the Eastern Himalayas, a
biological treasure trove now threatened by climate change. A decade of research carried
out by scientists in remote mountain areas endangered by rising global temperatures
brought exciting discoveries such as a bright green frog that uses its red and long webbed
feet to glide in the air. One of the most significant findings was not exactly
“new” in the classic sense. A 100-million year-old gecko, the oldest fossil
gecko species known to science, was discovered in an amber mine in the Hukawng Valley in
the northern Myanmar. The WWF report The Eastern Himalayas – Where Worlds Collide
details discoveries made by scientists from various organizations between 1998 and 2008 in
a region reaching across Bhutan and north-east India to the far north of Myanmar as well
as Nepal and southern parts of Tibet Autonomus Region (China).
Taking the Needle's Sting Out of
Diabetes
Found in 30% of all human cancer tumors, the Ras protein literally "drives cells
crazy," says Prof. Yoel Kloog, the dean of the Faculty of Life Sciences at Tel Aviv
University. Prof. Kloog was the first in the world to develop an effective anti-Ras drug
against pancreatic cancer, currently in clinical trials. Now, new research published in
the June issue of the European Journal of Pharmacology shows that the drug might be able
to slow the progression of diabetes as well. Prof. Kloog's student Adi Mor of TAU's
Department of Neuro-biochemistry and Sackler School of Medicine has modified Prof. Kloog's
anti-Ras FTS compound to develop what could be the first tablet-based treatment for
children and adults with Type 1 diabetes. Early results show that FTS is effective in
restoring insulin production in animal models — which could spell an end to the daily
needle injections endured by diabetics. "Our anti-Ras compound has shown very
positive results in inhibiting diabetes," says Mor. And given the drug's history
— FTS has already passed toxicity studies for other diseases and disorders — it
has the potential to fast-track through FDA regulatory hurdles, skipping straight to Phase
II clinical trials. A new drug for diabetes could be ready in as little as five years'
time.
New Discovery Brings Hope to
Treatment of Lymphatic Diseases
Researchers in the laboratory of Dr. Jayakrishna Ambati at the University of Kentucky have
discovered the first naturally occurring molecule that selectively blocks lymphatic vessel
growth. In an article in the Aug. 9, 2009 online edition of Nature Medicine, they report
the identification of a new molecule known as soluble VEGFR-2 that blocks
lymphangiogenesis – the growth of lymphatics – but not blood vessel growth. The
twin circulatory systems of mammals - blood and lymphatic - are intricately intertwined,
both anatomically and functionally. Until now it has been difficult to selectively target
one without affecting the other. The lymphatic vessel network is essential for
transporting fluids, molecules, and immune cells. It is crucial for wound healing and
immune defense. Disturbances in the lymphatics are involved in diseases as varied as
lymphedema, transplant rejection, and tumor metastasis, which collectively affect hundreds
of millions of people worldwide. This article, whose lead author is Dr. Romulo
Albuquerque, currently a medical student in the UK College of Medicine, showed that
soluble VEGFR-2 specifically blocks lymphatic vessel growth both during development and
following injury by blocking VEGF-C, a powerful lymphatic growth factor. It also reports
that loss of soluble VEGFR-2 during development led to the spontaneous invasion of
lymphatic vessels, but not blood vessels, into the cornea, solving the long-standing
mystery of why the cornea is normally devoid of lymphatics. Soluble VEGFR-2 was also
required for normal development of lymphatics in the skin.
New groundbreaking treatment for
oxygen-deprived newborns
Until now immediate cooling of the newborn infant was the only treatment that could
possibly prevent brain damage following oxygen deprivation during delivery. New research
findings from the Sahlgrenska Academy and Sahlgrenska University Hospital, in
collaboration with Zhengzhou University in China, open up the possibility of a new and
effective treatment that can be started as late as two days after birth. This new
treatment involves newborn infants being given a two-week course of injections of
erythropoietin, a hormone that stimulates the formation of red blood cells. “For the
first time we can demonstrate that it is possible to influence the brain damage occurring
as a result of oxygen deprivation during delivery considerably later than the six-hour
window of opportunity for treating with cooling,” says Klas Blomgren, professor of
paediatrics at the Sahlgrenska Academy and specialist at Queen Silvia Children’s
Hospital.
The ugly truth about one night
stands
Men are far more interested in casual sex than women. While men need to be exceptionally
at-tractive to tempt women to consider casual sex, men are far less choosy. These
findings1 by Dr Achim Schützwohl, from the Department of Psychology at Brunel University
in the UK, and his team are published online in Springer’s journal Human Nature.
UT Southwestern physicians bust
myths about insulin
People diagnosed with type 2 diabetes often resist taking insulin because they fear
gaining weight, developing low blood sugar and seeing their quality of life decline. A
study recently completed at UT Southwestern Medical Center suggests that those fears are
largely unfounded and that patients and physicians should consider insulin as a front-line
defense, as opposed to a treatment of last resort for non-insulin-dependent diabetes.
“We found that those patients who received insulin initially did just as well, if not
better, than those who didn’t receive insulin,” said Dr. Ildiko Lingvay,
assistant professor of internal medicine at UT Southwestern and lead author of the study
appearing online and in a future issue of Diabetes Care. “This reinforces the idea
that insulin treatment is a viable and safe option for patients, even in the very initial
stages of their diagnoses.
What Science Says About Beach Sand
and Stomach Aches
By washing your hands after digging in beach sand, you could greatly reduce your risk of
ingesting bacteria that could make you sick. In new research, scientists have determined
that, although beach sand is a potential source of bacteria and viruses, hand rinsing may
effectively reduce exposure to microbes that cause gastrointestinal illnesses. “Our
mothers were right! Cleaning our hands before eating really works, especially after
handling sand at the beach,” said Dr. Richard Whitman, the lead author of the U.S.
Geological Survey (USGS) study. “Simply rinsing hands may help reduce risk, but a
good scrubbing is the best way to avoid illness.” For this study, scientists measured
how many E. coli bacteria could be transferred to people’s hands when they dug in
sand. They analyzed sand from the shores of Lake Michigan in Chicago. Using past findings
on illness rates, scientists found that if individuals were to ingest all of the sand and
the associated biological community retained on their fingertip, 11 individuals in 1000
would develop symptoms of gastrointestinal illness. Ingestion of all material on the
entire hand would result in 33 of 1000 individuals developing gastrointestinal illness. In
a further laboratory experiment, USGS scientists determined that submerging one’s
hands four times in clean water removed more than 99% of the E. coli and associated
viruses from the hands.
Discovery may lead to powerful new
therapy for asthma
University of Texas Medical Branch at Galveston researchers have found that a single
enzyme is apparently critical to most allergen-provoked asthma attacks — and that
activity of the enzyme, known as aldose reductase, can be significantly reduced by
compounds that have already undergone clinical trials as treatments for complications of
diabetes. The discovery, made in experiments conducted with mice and in human cell
cultures, opens the way to human tests of a powerful new treatment for asthma, which today
afflicts more than 20 million Americans. Such a development would provide a badly needed
alternative to current asthma therapy, which primarily depends on hard-to-calibrate
inhaled doses of corticosteroids and bronchodilators, which have a number of side effects.
"Oral administration of aldose reductase inhibitors works effectively in experimental
animals," said UTMB professor Satish Srivastava, senior author of a paper on the
discovery appearing in the Aug. 6 issue of the journal PLoS One. "If these drugs work
as well in humans as they do in animals you could administer them either orally or in a
single puff from an inhaler and get long-lasting results." Srivastava and his
colleagues (postdoctoral fellows Umesh Yadav and Leopoldo Aguilera-Aguirre, associate
professor Kota Venkata Ramana, professor Istvan Boldogh and LSU Health Sciences Center
assistant professor Hamid Boulares) focused on aldose reductase inhibition as a possible
asthma therapy after establishing an essential role for the enzyme in other diseases also
characterized by inflammation. In disorders such as colon cancer, atherosclerosis, sepsis
and uveitis, the Srivastava team has found, cells are hit by a sudden overload of reactive
oxygen species (varieties of oxygen and oxygen compounds that are especially eager to
react with other molecules). The result is a chain of biochemical reactions that leads the
cells' genetic machinery to crank out a barrage of inflammatory signaling proteins. These
summon immune system cells and generate even more reactive oxygen species, producing a
vicious cycle of ever-increasing inflammation.
Oxygen treatment hastens memory
loss in Alzheimer's mice
A 65-year-old women goes into the hospital for routine hip surgery. Six months later, she
develops memory loss and is later diagnosed with Alzheimer's Disease. Just a coincidence?
Researchers at the University of South Florida and Vanderbilt University don't think so.
They suspect that the culprit precipitating Alzheimer's disease in the elderly women may
be a routine administration of high concentrations of oxygen for several hours during, or
following, surgery – a hypothesis borne out in a recent animal model study. Dr. Gary
Arendash of the Florida Alzheimer's Disease Research Center at USF and Dr. L. Jackson
Roberts II at Vanderbilt University used mice genetically altered to develop abnormal
levels of the protein beta amyloid, which deposits in the brain as plaques and eventually
leads to Alzheimer's-like memory loss as the mice age. They found that young adult
Alzheimer's mice exposed to 100-percent oxygen during several 3-hour sessions demonstrated
substantial memory loss not otherwise present at their age. Young adult Alzheimer's mice
exposed to normal air had no measurable memory loss, and neither did normal mice without
any genetic predisposition for Alzheimer's disease. The authors suggest that people
genetically predisposed to Alzheimer's disease or with excessive amounts of beta amyloid
in their brains are at increased risk of developing the disease earlier if they receive
high concentrations of oxygen, known as hyperoxia. Their study is published online this
month in NeuroReport. "Although oxygen treatment beneficially increases the oxygen
content of blood during or after major surgery, it also has several negative effects that
we believe may trigger Alzheimer's symptoms in those destined to develop the
disease," said USF neuroscientist Arendash, the study's lead author. "Our study
suggests that the combination of brain beta amyloid and exposure to high concentrations of
oxygen provides a perfect storm for speeding up the onset of memory loss associated with
Alzheimer's Disease."
UCF scientists control living cells
with light; advances could enhance stem cells' power
University of Central Florida researchers have shown for the first time that light energy
can gently guide and change the orientation of living cells within lab cultures. That
ability to optically steer cells could be a major step in harnessing the healing power of
stem cells and guiding them to areas of the body that need help. The results, presented at
the 2009 Conference on Lasers and Electro-Optics/International Quantum Electronics
Conference, were discovered by a research team led by Aristide Dogariu, an optical
scientist at the College of Optics and Photonics, and Kiminobu Sugaya, a stem cell
researcher at the College of Medicine's Burnett School of Biomedical Sciences. Long-term
implications of the work include stimulating and controlling tissue regeneration for
cleaner wound healing and the possibility of altering the shapes of cells and preventing
malignant tumors from spreading throughout the body. While optical techniques such as
drilling microscopic holes with light or using the light as tweezers have shown promise in
manipulating small pieces of matter, the UCF team explored the use of a gentler light
energy. Their work showed for the first time that optically induced torques can affect
components within cells that drive their motility -- their ability to move spontaneously
-- and change the orientation of cells within cultures. While earlier studies of cell
manipulation have emphasized shielding the cell from the power of the light, Dogariu and
Sugaya focused on using that energy to stimulate the cells' natural tendencies.
A new study by researchers at Wake Forest University School of Medicine may reveal how
long-lasting memories form in the brain. The researchers hope that the findings, now
available online and scheduled to appear in an upcoming issue of Neuroscience, may one day
help scientists develop treatments to prevent and treat conditions such as post-traumatic
stress disorder. "Although many things are known about memories that form from repeat
experiences, not much is known with regard to how some memories form with just one
exposure," said Ashok Hegde, Ph.D., an associate professor of neurobiology and
anatomy and the lead investigator on the study. Scientists do know that people tend to
remember extremely happy or sad occasions vividly because of the emotional connection,
Hegde said. Extreme emotions trigger the release of a chemical in the brain called
norepinephrine, which is related to adrenaline. That norepinephrine somehow helps memories
last a long time – some even a lifetime. For example, he said, when a person asks,
"Where were you when the 9/11 attacks happened?" most people can recall
immediately where they were and what they were doing when they heard the news. They
remember the moment as if it just happened because a national tragedy arouses emotion and
emotion somehow makes memories last for a long time, Hegde explained.
UCLA researchers determine toxic
levels of Alzheimer's clusters in brain
Scientists have long suspected that Alzheimer's disease (AD) is caused by a small protein
called the amyloid ?-protein (A?). This protein clumps or binds to itself, eventually
changing chemically to create brain protein deposits (plaques) that are characteristic of
AD. However, recent studies have suggested that it is not the plaques that cause AD but
rather these small, grape-like clusters of A?. These clusters vary in size, and the
relationship between cluster size and their ability to kill nerve cells (toxicity) has
never been determined accurately. Until now. By creating various sizes of A? clusters in
the lab that exactly match what forms in brains of those afflicted with AD, neurologists
at UCLA have determined that toxicity increases dramatically as clusters increase in size
from two to three to four A?s. The researchers also report that although the larger
clusters are more toxic than smaller ones, the larger formations are relatively rare;
smaller versions are numerous and thus are an inviting target for the development of new
therapeutic drugs. In addition, said David Teplow, senior author and a professor of
neurology, developing the ability to make A? clusters in a very pure and precise way that
duplicates what forms in AD brains will enable scientists to make detailed studies of
their structures. This too will make development of future therapeutic drugs much easier
and likely more successful. The research appears in the early on line edition of the
Proceedings of the National Academy of Sciences (PNAS). Alzheimer's disease is the most
common form of late-life dementia. More then five million Americans have been diagnosed
with the disease, 24 million worldwide, and the numbers are expected to reach 81 million
by the year 2040. "We now have the best understanding yet of what types of toxic
A-beta structures we should target with new classes of therapeutic drugs," said
senior author David Teplow, a professor of neurology at UCLA.
McGill/JGH researchers successfully
reverse multiple sclerosis in animals
A new experimental treatment for multiple sclerosis (MS) completely reverses the
devastating autoimmune disorder in mice, and might work exactly the same way in humans,
say researchers at the Jewish General Hospital Lady Davis Institute for Medical Research
and McGill University in Montreal. MS is an autoimmune disease in which the body's own
immune response attacks the central nervous system, almost as if the body had become
allergic to itself, leading to progressive physical and cognitive disability. The new
treatment, appropriately named GIFT15, puts MS into remission by suppressing the immune
response. This means it might also be effective against other autoimmune disorders like
Crohn's disease, lupus and arthritis, the researchers said, and could theoretically also
control immune responses in organ transplant patients. Moreover, unlike earlier
immune-supppressing therapies which rely on chemical pharamaceuticals, this approach is a
personalized form of cellular therapy which utilizes the body's own cells to suppress
immunity in a much more targeted way. GIFT15 was discovered by a team led by Dr. Jacques
Galipeau of the JGH Lady Davis Institute and McGill's Faculty of Medicine. The results
were published August 9 in the prestigious journal Nature Medicine. GIFT15 is composed of
two proteins, GSM-CSF and interleukin-15, fused together artificially in the lab. Under
normal circumstances, the individual proteins usually act to stimulate the immune system,
but in their fused form, the equation reverses itself.
Researchers from Boston University School of Medicine (BUSM) have found that individuals
who have a long history of alcoholism, but who have been abstinent for at least a month up
to many years, showed abnormal brain activity when looking at facial expressions of
others. The findings, which appear in the August 11 issue of Alcoholism: Clinical and
Experimental Research, confirms that alcoholics suffer from abnormalities in parts of the
brain that control emotional perception and memory. The emotional changes experienced by a
long-term chronic alcoholic cover a broad spectrum. Some of these changes, apathy and
emotional flatness are reminiscent of those seen in patients with bilateral frontal lobe
damage or in patients with right-hemisphere damage. Other abnormalities are subtle. For
example, alcoholics may make atypical judgments regarding the nature of facial emotional
expressions, suggesting that alcoholism may involve an underlying neurocognitive deficit
in the capacity to comprehend emotional information. In this study, researchers compared
abstinent long-term alcoholics to healthy nonalcoholic controls by using functional
magnetic resonance imaging (fMRI) that focused on abnormalities in temporal limbic
(amygdala and hippocampus) brain activation to emotionally expressive faces. Employing
both verbal (word) and non-verbal (face) materials in an effort to contrast relative
hemispheric sensitivities to the cumulative effects of alcohol abuse, the researchers
found abstinent long-term alcoholics showed decreased and abnormal brain activity when
looking at facial expressions, in particular in the amygdala and hippocampus areas of the
brain. Interview Ghislaine Lanctot
on vaccin maffia
Michael Pritchard's water filter
turns filthy water drinkable
Too much of the world lacks access to clean drinking water. Engineer Michael Pritchard
did something about it -- inventing the portable Lifesaver filter, which can make the most
revolting water drinkable in seconds. An amazing demo from TEDGlobal 2009.
Tip: Jan van Vlerken
FOOD, INC. — ReThink Review
Imagine a world where the food you ate was secretly replaced with a factory-created
artificial replica that looked, smelled, and tasted just like the original, sometimes even
better. But most of this fake food, including the meat, was made of only one or two
plant-based materials and a gang of weird chemicals, and if you ate enough of it, it would
slowly kill you through a range of terrible diseases. Well guess what America? You
currently live in such a bizarro world! The nearly complete industrialization and
corporatization of our food system is one of America's darkest, deadliest, and best-kept
secrets, and the important new documentary FOOD, INC. seeks to expose it by asking
questions you'd think we'd already have the answers to — how is our food made, who's
making it, and what the hell are they putting in it?
How To Brainwash A Nation - Ex-KGB
This amazing interview was done back in 1985 with a former KGB agent who was trained in
subversion techniques. He explains the 4 basic steps to socially engineering entire
generations into thinking and behaving the way those in power want them to. It's shocking
because our nation has been transformed in the exact same way, and followed the exact same
steps.
A feature length documentary about the origins of the modern environmental movement,
told through the eyes of nine Americans who were inspired to act on what they believed was
the most important challenge facing mankind. The film opens in the 1950s when a small
group of scientists began to document the impact of our technology on the Earths ecosystem
Antibodies to strep throat bacteria
linked to obsessive compulsive disorder in mice
A new study by researchers at Columbia University Mailman School of Public Health's Center
for Infection and Immunity indicates that pediatric obsessive-compulsive disorder (OCD),
Tourette syndrome and/or tic disorder may develop from an inappropriate immune response to
the bacteria causing common throat infections. The mouse model findings, published online
by Nature Publishing Group in this week's Molecular Psychiatry, support the view that this
condition is a distinct disorder, and represent a key advance in tracing the path leading
from an ordinary infection in childhood to the surfacing of a psychiatric syndrome. The
research provides new insights into identifying children at risk for autoimmune brain
disorders and suggests potential avenues for treatment. OCD and tic disorders affect a
significant portion of the population. More than 25% of adults and over 3% of children
manifest some features of these disorders. Until now, scientists have been unable to
convincingly document the association between the appearance of antibodies directed
against Group A beta-hemolytic streptoccoccus (GABHS) in peripheral blood and the onset of
the behavioral and motor aspects of the disorder. As a result, treatment strategies were
restricted to targeting symptoms rather than causes. Strep throat bacteria, or GABHS, are
known to cause autoimmune disorders such as Sydenham chorea, with symptoms such as fever
and uncontrolled tics of the face or extremities in susceptible individuals, prompting
some scientists to suspect that GABHS could play a role in a syndrome known as Pediatric
Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections (PANDAS), a
rapid-onset and episodic form of OCD and tic disorders observed in some children. The
latest study by CII researchers supports the hypothesis that some neuropsychiatric
syndromes may be triggered by direct action of GABHS-associated antibodies on the brain.
Whether environmental factors other than GABHS can lead to similar effects is as yet
unknown.
Aspirin use after colorectal cancer
diagnosis associated with improved survival
Men and women who were diagnosed with colorectal cancer and began regular use of aspirin
had a lower risk of overall and colorectal cancer death compared to patients not using
aspirin, according to a study in the August 12 issue of JAMA. Numerous prospective,
observational studies demonstrate that regular aspirin use is associated with a lower risk
of colorectal adenoma (a benign tumor) or cancer. Aspirin is likely, at least in part, to
prevent colorectal neoplasia (tumor growth) through inhibition of cyclooxygenase-2 (COX-2;
an enzyme), which promotes inflammation and cell proliferation, and is overexpressed in
the majority of human colorectal cancers, according to background information in the
article. However, the influence of aspirin on survival after diagnosis of colorectal
cancer has been unknown. Andrew T. Chan, M.D., M.P.H., of Massachusetts General Hospital
and Harvard Medical School, Boston, and colleagues studied the association between aspirin
use and survival among 1,279 men and women with nonmetastatic (stage I, II, and III)
colorectal cancer who were participating in 2 large prospective cohort studies (Nurses'
Health Study [NHS] and the Health Professionals Follow-up Study [HPFS]) that were
initiated (in 1980 and 1986, respectively) prior to cancer diagnosis and followed up
through June 1, 2008. "Within these cohorts, we previously have demonstrated that
regular aspirin use was associated with a reduction in the subsequent risk of developing
an initial primary colorectal cancer, particularly tumors with COX-2 overexpression.
Because these participants have provided biennially updated data on aspirin use, we had a
unique opportunity to extend these findings by examining the influence of prediagnosis and
postdiagnosis aspirin use on the survival of patients with established colorectal
cancer," the authors write.
Mediterranean diet, physical
activity linked with lower risk of Alzheimer disease
Elderly individuals who had a diet that included higher consumption of fruits, vegetables,
legumes, cereal and fish and was low in red meat and poultry and who were physically
active had an associated lower risk of Alzheimer disease, according to a study in the
August 12 issue of JAMA. In a second study, higher adherence to a Mediterranean diet was
associated with slower cognitive decline, but was not associated with a decreased risk of
dementia. Research regarding the effect physical activity can have on the risk of
Alzheimer disease (AD) or dementia has shown mixed results, as has the effect of dietary
habits. Their combined association has not been investigated, according to background
information in the article. Nikolaos Scarmeas, M.D., of Columbia University Medical
Center, New York, and colleagues examined the association between physical activity and
risk of AD and also the effect of physical activity and adherence to a Mediterranean-type
diet on AD risk. The study included 2 groups that consisted of 1,880 community-dwelling
elderly residents of New York city without dementia at the start of the study, for whom
there was both diet and physical activity information available. Standardized neurological
and neuropsychological measures were administered approximately every 1.5 years from 1992
through 2006. The participants received measurements of their adherence to a
Mediterranean-type diet (scale of 0-9; categorized as low, middle, or high) and their
physical activity (sum of weekly participation in various physical activities, weighted by
the type of physical activity [light, moderate, vigorous]; categorized into no physical
activity, some, or much, also low or high), separately and combined. A higher score for
diet was obtained with higher consumption of fruits, vegetables, legumes, cereals, and
fish; lower consumption of meat and dairy products; a higher ratio of monounsaturated fats
to saturated fats and mild to moderate alcohol consumption. Individuals were followed up
for an average of 5.4 years, during which a total of 282 developed AD. In considering only
physical activity, the researchers found that more physical activity was associated with
lower risk for developing AD. "Compared with physically inactive individuals, report
of some physical activity was associated with a 29 percent to 41 percent lower risk of
developing AD, while report of much physical activity was associated with a 37 percent to
50 percent lower risk," the authors write.
A synthetic derivative of the kudzu
vine can reduce drinking and prevent relapse
Kudzu and its extracts and flowers have been used in traditional Chinese folk medicine to
treat alcoholism for about 1,000 years. Kudzu contains daidzin, an anti-drinking
substance. Daidzin inhibits human aldehyde dehydrogenase 2 (ALDH-2), which metabolizes
alcohol into acetaldehyde. Inhibiting ALDH-2 promotes the accumulation of acetaldehyde,
which has aversive effects. A recent test of a synthetic ALDH-2 inhibitor (CVT-10216) on
rodents shows that it reduces drinking and prevents relapse by increasing acetaldehyde
while drinking and later decreasing dopamine in the brain region that controls relapse
during abstinence.Results will be published in the November issue of Alcoholism: Clinical
& Experimental Research and are currently available at Early View. "I think the
over-arching issue here is medical treatment," said Ivan Diamond, vice president of
neuroscience at Gilead Science, Professor Emeritus of neurology, cellular and molecular
pharmacology and neuroscience at the University of California, San Francisco, and
corresponding author for the study.
Traffic jam in brain causes
schizophrenia symptoms
Schizophrenia waits silently until a seemingly normal child becomes a teenager or young
adult. Then it swoops down and derails a young life. Scientists have not understood what
causes the severe mental disorder, which affects up to 1 percent of the population and
results in hallucinations, memory loss and social withdrawal.But new research from the
Northwestern University Feinberg School of Medicine has revealed how schizophrenia works
in the brain and provided a fresh opportunity for treatment. In a new, genetically
engineered mouse model, scientists have discovered the disease symptoms are triggered by a
low level of a brain protein necessary for neurons to talk to one another. In human and
mouse brains, kalirin is the brain protein needed to build the dense network of highways,
called dendritic spines, which allow information to flow from one neuron to another.
Northwestern scientists have found that without adequate kalirin, the frontal cortex of
the brain of a person with schizophrenia only has a few narrow roads. The information from
neurons gets jammed up like rush hour traffic on an interstate highway squeezed to a
single lane. "Without enough pathways, the information takes much longer to travel
between neurons and much of it will never arrive," said Peter Penzes, assistant
professor of physiology at the Feinberg School. He is senior author of a paper reporting
the findings published in a recent issue of the Proceedings of the National Academy of
Science. Michael Cahill, a Feinberg doctoral student in neuroscience, is the lead author.
Insufficient sleep may be linked to
increased diabetes risk
Short sleep times, experienced by many individuals in Westernized societies, may
contribute to the development of insulin resistance and reduced glucose tolerance, which
in turn may increase the long-term risk of diabetes, according to a new study accepted for
publication in The Endocrine Society's Journal of Clinical Endocrinology & Metabolism
(JCEM). Sleep curtailment is an increasingly common aspect of the Western lifestyle, which
is characterized by physical inactivity and overeating. Today, many Americans sleep fewer
than six hours each night and individuals who report such short sleep times have in
previous studies demonstrated an increased risk of developing diabetes. This new study
examined whether reduced sleep duration itself may increase the risk of developing
diabetes when combined with physical inactivity and overeating. Researchers in this study
subjected a group of healthy middle-aged men and women to two controlled 14-day periods of
sedentary living with free access to food and 5.5 or 8.5 hour bedtimes. When the subjects
had their bedtimes decreased from 8.5 hours to 5.5 hours they showed changes in their
response to two common sugar tests, which were similar to those seen in people with an
increased risk of developing diabetes. "Our findings raise the possibility that when
the unhealthy aspects of the Westernized lifestyle are combined with reduced sleep
duration, this might contribute to the increased risk of many overweight and sedentary
individuals developing diabetes," said Plamen Penev, MD, PhD, of the University of
Chicago and a senior author of the study. "If confirmed by future larger studies,
these results would indicate that a healthy lifestyle should include not only healthy
eating habits and adequate amounts of physical activity, but also obtaining a sufficient
amount of sleep."
Endocrine Society Calls for
Medicare Coverage of DXA Bone Density Testing to be Extended to Men with Testosterone
Deficiency
Hypogonadism, also known as testosterone deficiency, affects 4-5 million men in the United
States placing them at risk for developing osteoporosis. Despite the clear association of
testosterone deficiency with low bone density and osteoporosis, Medicare does not provide
coverage for bone density testing for these individuals. To address this concern, today
The Endocrine Society issued a Position Statement, endorsed by the National Osteoporosis
Foundation, calling for Medicare coverage of bone density testing to be extended to this
at-risk population. Bone mineral density, measured by dual energy x-ray absorptiometry
(DXA), is an excellent predictor of the risk of fractures in both men and women.
Nationally, Medicare currently provides coverage for DXA scans in men only when an
individual has been previously diagnosed with osteoporosis, osteopenia or has had a
vertebral bone fracture. This means that most men found to have osteoporosis are diagnosed
only after a hip or spine fracture has already occurred.
Worth the effort? Not if you're
depressed
New research indicates that decreased cravings for pleasure may be at the root of a core
symptom of major depressive disorder. The research is in contrast to the long-held notion
that those suffering from depression lack the ability to enjoy rewards, rather than the
desire to seek them. The research, led by Vanderbilt psychologists Michael Treadway and
David Zald, was published Aug. 12 by the online journal PLoS One. "This initial study
shows that decreased reward processing, which is a core symptom of depression, is
specifically related to a reduced willingness to work for a reward," Treadway, a
graduate student in psychology, said. Decreased motivation to seek and experience
pleasurable experiences, known as anhedonia, is a primary symptom of major depressive
disorder. Anhedonia is less responsive to many antidepressants and often persists after
other symptoms of depression subside. However, understanding the different components of
anhedonia - the desire to obtain something pleasurable versus experiencing pleasure - has
been difficult for researchers to determine in humans. "In the last decade and a
half, animal models have found that the neurotransmitter dopamine, long known to be
involved in reward processing, is involved in craving or motivation, but not necessarily
enjoyment," Treadway said. "To date, research into reward processing in
individuals with anhedonia has focused on enjoyment of rewards, rather than assessing the
drive to work for them. We think this task is one of the first to do that."
Fungus Found in Humans Shown To Be
Nimble in Mating Game
Brown University researchers have discovered that Candida albicans, a human fungal
pathogen that causes thrush and other diseases, pursues same-sex mating in addition to
conventional opposite-sex mating. Scientists have observed this same-sex mode of
reproduction in other fungi, but this is the first time they have identified it in Candida
albicans, the most common human fungal pathogen.
Researchers identify potential new
avenue to attack cancer
New insight into how human cells reproduce, published by cancer researchers at Michigan
State University and the Van Andel Research Institute in Grand Rapids, could help
scientists move closer to finding an “off switch” for cancer. Cancer cells
divide uncontrollably and can move from one part of the body to another. They undergo
dramatic shifts in shape when they do so, said Aaron DeWard, an MSU cell and molecular
biology doctoral candidate who published his research recently in the Journal of
Biological Chemistry. He’s trying to figure out how certain proteins trigger cell
movement and division and how cancer hijacks the system to create genomic instability.
DeWard and his academic adviser, VARI senior scientific investigator Art Alberts,
investigated proteins called formins that help determine the shape of a cell during
division and movement. They identified a new mechanism for regulation of formins during
cell division.
A Window into the Brain
When we absorb new information, the human brain reshapes itself to store this newfound
knowledge. But where exactly is the new knowledge kept, and how does that capacity to
adapt reflect our risk for Alzheimer's disease and other forms of senile dementia later in
our lives? Dr. Yaniv Assaf of Tel Aviv University's Department of Neurobiology is
pioneering a new way to track the effect of memory on brain structure. "With a
specific MRI methodology called 'Diffusion Imaging MRI,' we can investigate the
microstructure of the tissue without actually cutting into it," he explains. "We
can measure how much capacity our brain has to change structurally, what our memory
reserve is and where that happens."
Hebrew U. researchers shed light on
the brain mechanism responsible for processing of speech
Researchers from the Hebrew University of Jerusalem have succeeded for the first time in
devising a model that describes and identifies a basic cellular mechanism that enables
networks of neurons to efficiently decode speech in changing conditions. The research may
lead to the upgrading of computer algorithms for faster and more precise speech
recognition as well as to the development of innovative treatments for auditory problems
among adults and young people. Our brain has the capability to process speech and other
complex auditory stimuli and to make sense of them, even when the sound signals reach our
ears in a slowed, accelerated or distorted manner.
Scientists Find New No-Needle
Approach to Prevent Blood Clots
The dean of the University of Oklahoma College of Public Health and a team of scientists
worldwide have found a better way to prevent deadly blood clots after joint replacement
surgery – a major problem that results in thousands of unnecessary deaths each year.
The research appears this week in the New England Journal of Medicine. The research team,
which includes scientists from Oklahoma, Denmark, Australia and Canada, set out to find a
better way to prevent blood clots without increasing the risk of bleeding. Blood clots,
known as deep-vein thrombosis (DVT), affect the large veins in the lower leg and thigh. If
the clot breaks free and moves through the bloodstream, it can lodge in the lungs, a
condition known as pulmonary embolism (PE), which is often fatal. Pulmonary embolism is
the most common preventable cause of sudden death after surgery. Current preventive
treatments include uncomfortable injections and one oral anti-clotting medicine that is
difficult for patients and physicians to manage. Researchers wanted to find something
better.
Uncovering the secrets of
ulcer-causing bacteria
A team of researchers from Boston University, Harvard Medical School and Massachusetts
Institute of Technology recently made a discovery that changes a long held paradigm about
how bacteria move through soft gels. They showed that the bacterium that causes human
stomach ulcers uses a clever biochemical strategy to alter the physical properties of its
environment, allowing it to move and survive and further colonize its host. The
Proceedings of the National Academy of Sciences reports the findings in its most recent
issue. Helicobacter pylori is a bacterium that inhabits various areas of the stomach where
it causes chronic, low-level inflammation and is linked to gastric ulcers and stomach
cancer. In order to colonize the stomach, H. pylori must cope with highly acidic
conditions in which other bacteria are unable to survive. It is well known however, that
the bacterium accomplishes this by producing ammonia to neutralize the acid in its
surroundings. In addition, newly published research shows it does something else; it
changes its environment to enable freer movement. Acidic conditions within the stomach
also work against the bacteria's ability to move freely. This is due to a protein called
"mucin," a crucial component of the protective mucus layer in the stomach. In
the presence of acid mucin forms a protective gel, which acts as a physical barrier that
stops harmful bacteria from reaching the cell wall. But, H. pylori increases the pH of its
surroundings and changes this "mucin" gel to a liquid, allowing the bacterium to
swim across the mucus barrier, establish colonies, attack surface cells and form ulcers.
"Bacteria 'swim' through watery fluids using their tails to propel them," said
Boston University physicist Rama Bansil, who is currently on leave from BU, working as a
Division of Materials Research program manager at the National Science Foundation.
"But it was not obvious how they move through a soft gel like mucus."
Scientists demonstrate importance
of niche differences in biodiversity
Scientists at UC Santa Barbara have found strong evidence that niche differences are
critical to biodiversity. Their findings are published online in this week's issue of the
journal Nature. "Ecologists have long assumed that species differences in how they
use the environment are key to explaining the large number of species we see all around
us, but the importance of such niches have never been field tested," said first
author Jonathan M. Levine, associate professor in UCSB's Department of Ecology, Evolution,
and Marine Biology. Levine and his co-author Janneke HilleRisLambers, a former
postdoctoral fellow at UCSB, who is now an assistant professor at the University of
Washington, did field testing of small plants. These plants were found in northern Santa
Barbara County on rocky outcrops, where diversity is very high. They used a combination of
mathematical techniques, as well as experimental approaches, to remove niche differences
from these experimental communities. "Our work is important because it resolves a
century-old biodiversity puzzle," said Levine. "Why doesn't the single best
competitor exclude all others in the community?"
Biological clocks of insects could
lead to more effective pest control
Researchers at Oregon State University have discovered that the circadian rhythms or
biological "clocks" in some insects can make them far more susceptible to
pesticides at some times of the day instead of others. With further research, the
scientists said, it may be possible to tap into this genetic characteristic, identify the
times that a target insect is most vulnerable to a specific pesticide, and use that
information to increase the effectiveness, reduce costs and decrease the amounts of
pesticide necessary for insect control. Approaches such as this may also be highly useful
in programs of "integrated pest management," the researchers said, which aim to
minimize pesticide use, prevent development of resistance to pesticides, and use a broad
range of physical or chemical control measures to enhance the long-term effectiveness of
an insect control program in crop agriculture. The findings were just published in PLoS
ONE, a professional journal, in work supported by the U.S. Department of Agriculture,
National Institutes of Health and National Science Foundation. "We found that it took
triple the dose of one pesticide to have the same lethal effect on fruit flies at the time
of day their defenses were strongest, compared to when they were weakest," said
Louisa Hooven, a postdoctoral fellow in the OSU Department of Zoology and lead author on
the study. "A different pesticide took twice the dose. This makes it pretty clear
that the time of day of an exposure to a pesticide can make a huge difference in its
effectiveness." In recent years, researchers have found that the genes which are
sensitive to the natural rhythms of day and night can have a wide range of biological
effects, on everything from fertility to feeding patterns, sleep, hormone production,
stress, productivity, medication effectiveness and many other functions. And they operate
in multiple cells in many or most plant and animal species, including humans.
Carnitine supplements reverse
glucose intolerance in animals
Supplementing obese rats with the nutrient carnitine helps the animals to clear the extra
sugar in their blood, something they had trouble doing on their own, researchers at Duke
University Medical Center report. A team led by Deborah Muoio (Moo-ee-oo), Ph.D., of the
Duke Sarah W. Stedman Nutrition and Metabolism Center, also performed tests on human
muscle cells that showed supplementing with carnitine might help older people with
prediabetes, diabetes, and other disorders that make glucose (sugar) metabolism difficult.
Carnitine is made in the liver and recycled by the kidney, but in some cases when this is
insufficient, dietary carnitine from red meat and other animal foods can compensate for
the shortfall. After just eight weeks of supplementation with carnitine, the obese rats
restored their cells' fuel- burning capacity (which was shut down by a lack of natural
carnitine) and improved their glucose tolerance, a health outcome that indicates a lower
risk of diabetes. These results offer hope for a new therapeutic option for people with
glucose intolerance, older people, people with kidney disease, and those with type 2
diabetes (what used to be called adult-onset diabetes). Muoio said that soon her team of
researchers will begin a small clinical trial of carnitine supplementation in people who
fit the profile of those who might benefit from additional carnitine – older people
(60 to 80 years) with glucose intolerance.
Breakthrough in Alzheimer's
research
A combination of proteins in the cerebrospinal fluid can reliably identify which patients
with early symptoms of dementia will subsequently develop full-blown Alzheimer's disease,
a research team at the University of Gothenburg, Sweden, has found in a major
international study. The results were published in this week's edition of the Journal of
the American Medical Association (JAMA). Alzheimer's is one of the most common dementia
disorders. Around 160,000 people in Sweden currently suffer from dementia, and an
estimated 60 per cent of them have Alzheimer's. "There is currently no medication
that can alter the course of the disease, but the medicines currently under development
will probably have the greatest effect if they are used from an early stage, so methods
are needed for early diagnosis of the disease," says Dr Niklas Mattsson, a member of
Kaj Blennow's group at the Institute of Neuroscience and Physiology at the University of
Gothenburg's Sahlgrenska Academy. Changes in the brain are reflected in the cerebrospinal
fluid (CSF) in the form of biomarkers. Previous smaller studies have shown that the
proteins beta-amyloid, tau and phosphorylated tau in the CSF can be used to make an early
diagnosis of Alzheimer's. Now Mattsson and colleagues at hospitals in Sweden, elsewhere in
Europe and the USA have confirmed this in a large multicentre study with more than 1,500
participants. "These methods make it easier to identify the disease, which is
essential for making a correct diagnosis early on," he says. "These biomarkers
may be useful both in research to develop new medicines and in point-of-care diagnostics,
where they can support clinical diagnostics."
Manganese damages the immune
response in marine animals
Hypoxia, or lack of oxygen, in bottom waters is a well known environmental problem. New
research at the University of Gothenburg adds to the list of ill effects: hypoxia leads to
increased levels of manganese, which damages the immune response in marine animals. Water
eutrophication and the resulting hypoxia is an ever-current issue, not least in connection
with summer algal blooms. A more recently acknowledged problem is that hypoxia, which
occurs when algae is broken down, increases the release of toxic metals from bottom
sediments. Researchers at the University of Gothenburg have found that one of these
metals, manganese, may damage the immune response in marine animals.
Category-specific brain
organization in sighted and blind humans
A new study finds a surprising similarity in the way neural circuits linked to vision
process information in both sighted individuals and those who have been blind since birth.
The research, published by Cell Press in the August 13th issue of the journal Neuron,
reveals that category-specific localized activation of a critical part of the visual
cortex does not require any prior visual experience and provides fascinating and valuable
insight into the evolutionary history of the human brain. The ability to recognize
visually presented objects relies on a critical neural pathway called the ventral stream.
Previous imaging studies of the human brain have demonstrated that the sight of nonliving
objects, such as tools and houses, activates different regions within the ventral stream
than the sight of living things, such as animals and faces. It is not known whether
category-specific neural responses in the ventral stream depend on visual experience. One
way to answer this question is to explore whether category-specific activation of the
ventral stream is observed in adults who have been blind since birth. Although previous
research with blind humans has shown that tactile exploration of objects or imagery of
object shape based on sound activates the ventral stream, it is not clear whether stimuli
from different conceptual domains activate localized regions within the ventral stream.
"In particular, it is unknown whether individuals who are blind since birth will show
differential responses in medial regions of the ventral stream when thinking about
nonliving things," says lead study author, Dr. Bradford Mahon, who is currently at
the Department of Brain and Cognitive Sciences at the University of Rochester.
"Similarly, it is unknown whether, in the absence of visual experience, stimuli
corresponding to living things will lead to differential responses in regions that show
the same category preference in sighted individuals."
Children with newly diagnosed
epilepsy at risk for cognitive problems
Children who have normal IQs before they experience a first seizure may also have problems
with language, memory, learning and other cognitive skills, according to a study published
in the August 12, 2009, online issue of Neurology®, the medical journal of the American
Academy of Neurology. "Our study highlights the importance of testing children with
epilepsy for possible cognitive problems soon after they are diagnosed with epilepsy in
order to avoid these issues affecting them later in life, especially if they have
additional risk factors," said study author Philip Fastenau, PhD, Professor of
Neurology at Case Western Reserve University School of Medicine and the Neurological
Institute of University Hospitals in Cleveland, OH. The research was done in collaboration
with Indiana University Purdue University in Indianapolis and Cincinnati Children's
Hospital Medical Center. The study involved 282 school-aged children with an IQ of at
least 70 who experienced their first seizure within the previous three months. They were
then compared to 147 of their siblings without seizures. Scientists looked at whether the
children with seizures also had other risk factors associated with cognitive problems,
including multiple seizures, use of epilepsy drugs, or signs of epilepsy on early tests of
brain waves. Of the children who experienced one seizure, 27 percent showed cognitive
difficulties at or near the time of the first seizure and 40 percent of children who had
additional risk factors showed signs of cognitive problems. A child with all four risk
factors was three times more likely to experience cognitive problems by the first clinic
visit compared to children who were seizure-free. The study also showed that children who
took epilepsy drugs had difficulties in processing speed, language, verbal memory and
learning compared to children who did not take any epilepsy drugs.
Perform non-radiation ERCP during
pregnancy
Hormonal changes during pregnancy increase the lithogenicity of bile and impair
gallbladder emptying, which create a favorable environment for gallstone formation.
Choledocholithiasis and consequent complications such as pancreatitis and cholangitis are
potentially fatal diseases for the mother and fetus. During pregnancy, the treatment is
usually conservative since surgery is associated with an increased rate of complications
such as preterm labor and spontaneous abortion. In choledocholithiasis, endoscopic
retrograde cholangiopancreatography (ERCP) is the first-line treatment of choice. However,
a clear-cut safe radiation dose for ERCP in pregnancy is still unknown.
What is alternative treatment for
irritable bowel syndrome when conventional therapy has failed?
IBS remains a common intestinal disorder causing significant discomfort and poor quality
of life in patients who have the diagnosis. TCAs have been shown to improve abdominal pain
in patients with IBS; however, there is insufficient evidence of global symptom relief.
The search for an optimal treatment to improve symptoms and quality of life in IBS remains
ongoing. A research article to be published on August 7, 2009 in the World Journal of
Gastroenterology addresses this question. In the randomized, controlled trial, the
efficacy of imipramine in the treatment of symptoms of irritable bowel syndrome (IBS) was
studied. Patients diagnosed with IBS who failed treatment with conventional therapy were
enrolled to receive a 12-week course of low-dose imipramine. The effects were recorded
periodically based on the patients' subjective sense of global relief and their responses
to a standardized quality-of-life questionnaire. The results were significant for showing
improvement in global symptoms during and after 12 weeks of therapy with the medication.
There was also notable improvement in general quality of life as measured by a
standardized questionnaire.
Arizona researchers have added another piece to the mounting body of evidence that
suggests during resuscitation efforts to treat patients in cardiac arrest, "passive
ventilation" significantly increases survival rates, compared to the widely practiced
"assisted ventilation." The study, published in an online edition of Annals of
Emergency Medicine, compared the numbers of patients who had suffered a cardiac arrest
outside a hospital setting and were resuscitated in the field by Emergency Medical
Services personnel. Rescuers used either bag-valve-mask ventilation, which forces air into
the patient's lungs, or facemasks with a continuous flow of oxygen, which work in a
similar fashion to those carried on airplanes in case the cabin pressure drops. Among the
1,019 adult out-of-hospital cardiac arrest patients in the analysis, 459 received passive
ventilation and 560 received bag-valve-mask ventilation. Neurologically normal survival
after witnessed cardiac arrest with a shockable heart rhythm was higher for the passive
oxygen flow method (38.2 percent) than bag-valve-mask ventilation (25.8 percent).
"These results are strikingly similar to earlier observations from Wisconsin, where
survival rates went up from 15 percent to 38 percent after paramedics abandoned the
official guidelines for the modified protocol that we developed," says Gordon A. Ewy,
MD, a co-author of the study and director of the Sarver Heart Center at The University of
Arizona College of Medicine. The Sarver Heart Center's Resuscitation Research Group
developed a modified protocol for treating out-of-hospital cardiac arrest called
Cardiocerebral Resuscitation, as opposed to Cardiopulmonary Resuscitation, which should be
reserved for respiratory arrest (such as near-drowning or drug overdose). Under the new
concept, first tested in Wisconsin, EMS personnel no longer intubated the patient for
ventilation. Instead, they applied a facemask delivering a continuous, low-pressure flow
of oxygen.
Missing Link to Cloud Formation
Found
The discovery of a previously unknown chemical compound in the atmosphere may help to
explain how and when clouds are formed. The discovery of the so called dihydroxyepoxides
(an aerosol-precursor), is reported in this week's issue of Science by a team comprising
of researchers from the California Institute of Technology (Caltech) and the University of
Copenhagen. Professor Henrik Kjærgaard from the Department of Chemistry at the University
of Copenhagen calls the new compounds a missing link in the formation of clouds. "We
know that aerosols are important in the formation of clouds but, we didn't know much about
how the aerosols themselves were formed. This new compound may be just what we were
looking for," says the professor who has recently moved from University of Otago, New
Zealand to fill his new appointment in Copenhagen. The new compound was originally found
when a team of researchers from Caltech mounted a measuring device known as a Chemical
Ionization Mass Spectrometer (CIMS) on an aeroplane, and flew it over the oaken forests of
Northern America.
Formal education lessens the impact
of Alzheimer’s disease – even if brain volume is already reduced
Researchers at the Department of Psychiatry, Klinikum rechts der Isar, Technische
Universität München, investigated the effects of formal education on the symptoms of
Alzheimer’s disease. They were able to show that education diminishes the impact of
Alzheimer’s disease on cognition even if a manifest brain volume loss has already
occurred. The results are published in the current issue of the Journal of
Alzheimer’s Disease (“Education attenuates the effect of medial temporal lobe
atrophy on cognitive function in Alzheimer’s disease: The MIRAGE Study,” Journal
of Alzheimer’s Disease, August 2009). Dr. Robert Perneczky, Department of Psychiatry
at Klinikum rechts der Isar explains: “We know that there is not always a close
association between brain damage due to Alzheimer’s disease and the resulting
symptoms of dementia. In fact, there are individuals with severe brain pathology with
almost no signs of dementia, whereas others with only minor brain lesions exhibit a
considerable degree of clinical symptoms.” These phenomena are often ascribed to the
theoretical concept of cognitive reserve. A high level of cognitive reserve results in a
strong individual resilience against symptoms of brain damage; cognitive reserve can
therefore be seen as protective against brain damage.
Genetic Causes of Schizophrenia
In collaboration with colleagues from across Europe, researchers from the University of
Copenhagen and the Mental Health Services in the Capital Region of Denmark have found
mutations in the human genome that lead to an increased risk of developing schizophrenia.
This discovery brings about a new understanding of the interplay between genes and the
environment, i.e. why some individuals with specific genetic variations in, for example,
the immune system are sensitive to a number of environmental factors (e.g. infections)
when it comes to developing schizophrenia. The findings have just been published in the
reputed scientific journal, Nature.
Important step in neutralizing
toxic cause of muscle disease
Cell biologists from the Radboud University Nijmegen Medical Centre (Nijmegen, the
Netherlands) describe a new approach to remove the toxic agent that causes the
neuromuscular disease myotonic dystrophy. Their findings are published in the scientific
journal The Proceedings of the National Academy of Sciences.Myotonic dystrophy, also
called Steinert's disease, is a heritable, neuromuscular disease with an incidence of
about one in 10,000. It is the most common muscular dystrophy in adults. Typical symptoms
are delayed relaxation of muscles (myotonia) and muscle wasting (dystrophy). Other organs
frequently involved in the disease are heart and brain. Currently, no cure is available.
The Radboud University Nijmegen Medical Centre (RUNMC) is a reference centre for myotonic
dystrophy in the Netherlands.
Food Stamp Use Linked To Weight
Gain, Study Finds
The U.S. Food Stamp Program may help contribute to obesity among its users, according to a
new nationwide study that followed participants for 14 years. Researchers found that the
average user of food stamps had a Body Mass Index (BMI) 1.15 points higher than non-users.
The link between food stamps and higher weight was almost entirely based on women users,
who averaged 1.24 points higher BMI than those not in the program, the study found. For an
average American woman, this would mean an increase in weight of 5.8 pounds. The study
also found that people’s BMI increased faster when they were on food stamps than when
they were not, and increased more the longer they were in the program.
STAT3 Gene Regulates Cancer Stem
Cells in Brain Cancer
In a study published online in advance of print in Stem Cells, Tufts researchers report
that the STAT3 gene regulates cancer stem cells in brain cancer. Cancer stem cells have
many characteristics of stem cells and are thought to be the cells that drive tumor
formation. The researchers report that STAT3 could become a target for cancer therapy,
specifically in Glioblastoma multiforme (GBM), a type of malignant and aggressive brain
tumor.Patients with Glioblastoma multiforme typically survive 12 to 14 months with
treatment. Treatment options include radiation, chemotherapy, and surgery. “When
STAT3 is inhibited, cancer stem cells in glioblastomas lose their stem-cell
characteristics permanently, suggesting that STAT3 regulates growth and self-renewal of
stem cells within glioblastomas. Strikingly, a single, acute treatment with STAT3
inhibitors was effective, implying that a STAT3 inhibitor could stop tumor
formation,” said senior author Brent Cochran, PhD, a professor at Tufts University
School of Medicine and a member of the cellular & molecular physiology program faculty
at the Sackler School of Biomedical Sciences at Tufts.
Estrogen-Dependent Switch Tempers
Killing Activity of Immune Cells
The sex hormone estrogen tempers the killing activity of a specific group of immune cells,
the cytotoxic T cells (CTLs), which are known to attack tumor cells and cells infected by
viruses. The key player in this process is a cytotoxic T cell molecule which has been
known for a long time and which scientists have named EBAG9. Cancer researchers Dr.
Constantin Rüder and Dr. Armin Rehm together with immunologist Dr. Uta Höpken of the Max
Delbrück Center for Molecular Medicine (MDC) Berlin-Buch and Charité – University
Medicine Berlin, Germany, have now unraveled the function of EBAG9. Modulated by estrogen,
EBAG9 tempers the activity of CTLs. In the absence of EBAG9, the activity of CTLs is
enhanced (Journal of Clinical Investigation, Vol. 119, No. 8, pp 2184-2203, August 3,
2009)*. The sex hormone estrogen plays a critical role in the regulation of growth and the
development of cells. It is also crucial for cell-type-specific gene expression in various
tissues. Deregulation of this system results in breast and ovarian cancer. Those tumors
are successfully treated with drugs such as tamoxifen. Researchers suggest that this drug
inhibits tumor growth by blocking the estrogen receptors of the tumor cells. However, up
to now it has been unclear what effect this inhibition has on the immune system. In a
previous study, Japanese researchers detected large amounts of EBAG9 in estrogen-dependent
tumors. Dr. Rehm and his colleagues wondered what effect elevated levels of estrogen would
have on cytotoxic T cells that attack tumors. They assumed that EBAG9 could transmit this
effect of estrogen and therefore wanted to know what would happen if they knocked out the
gene for EBAG9 in mice. After knocking out the gene for EBAG9, they found that in the
absence of EBAG9 the “brake” of the immune cells is loosened. The immune cells
can release much more of the tumor-killing enzymes than in the presence of EBAG9. The
deathly harbingers are stored in granules (secretory lysosomes) in the cytotoxic T cells.
They have greater quantities of these granules at their disposal once the blockage of the
immune cells through EBAG9 is lifted. These findings of the researchers in Berlin may also
explain why drugs like tamoxifen act on tumor cell growth. One argument is that once the
estrogen receptors of the tumor cells are inhibited by the drug, the sex hormone can no
longer promote tumor growth. At the same time EBAG9 can no longer inhibit the cytotoxic T
cells. The immune cells are ready to attack and destroy the tumor cells.
Pamela Ronald and Raoul Adamchak:
The Food of the Future
Raoul Adamchak - Raoul Adamchak is the Market Garden Coordinator at the UC Davis
Student Farm. The Market Garden provides experiential learning opportunities to students
interested in organic agriculture. Adamchak's educational activities include programs in
organic vegetable crop production, operating a CSA (community supported agriculture
project), participating in farmers markets, organic green house production, vegetable
variety trials, on-campus sales, equipment operation, and student-directed internships.
Adamchak worked for many years as a partner in Full Belly Farm and as an inspector of
organic farms, and has served as the president of the board of California Certified
Organic Farmers.
Inside the Womb
Revolutionary ultrasound imaging techniques allow this two-hour National Geographic
documentary to enter the wondrous world of a human fetus -- inside the womb. You'll follow
the incredible journey of a growing embryo from its inception as a single-celled organism
to the beginning of brain activity to the first heartbeat. Soon the baby's senses start
developing, leading to a grand finale that's a real eye opener.
Google Me - now on iTunes!
Trailer for the film; Jim Killeen Googled his own name and made a documentary about the
men with whom he shares it.
Biofuels scandal + food prices
Why biofuel industry is dead -- biofuel by converting food into oil is stupid and
immoral. Biodiesel, biomass, biowaste and sugar to fuel conversion into biofuels. Foor
price rises. World bank report on biofuels and food prices. Ethanol and gasoline or petrol
mix, European Union EU policy changes on biofuel. Biofuels policy reversal. Anti-biofuel
campaigns. Biofuel blamed for food riots, hunger, food shortages, rising food prices,
wheat prices, food hoarding and stockpiles. Biofuel production: speculation in food
futures. Biofuel links oil price to food price. Do biofuel quotas cause starvation, Africa
Asia, India, China? Competition from biofuel manufafturers for food -- poor people cannot
eat, food prices rise, biofuel means burning wheat in car engines, driving vehicles on
biofuel, adding ethanol to petrol / gasoline. Biodiesel, soybean price rises, rice price
rises, food riots, biofuel destruction of forests for agriculture. Non biofuel reasons for
rising food prices: drought, crop failure, hoarding, ban on food exports, stockpiling of
food, speculation on food commodities markets. Ethics of biomass fuel generation and
increased use of fertilisers.
Poison on the Platter
Renowned filmmaker and social activist Mahesh Bhatt today launched a scathing attack on
biotech multinational companies and their nexus with regulatory bodies for unleashing what
he describes as 'bio-terrorism' in the country. Speaking at a function organized to launch
his new film, 'Poison on the Platter', directed by Ajay Kanchan, Bhatt said, "in
their mad rush to capture the multi-billion dollar Indian agricultural and food industry,
the biotech MNCs are bulldozing warnings by scientists about the adverse impact of GM
foods on health and environment, and hurtling the mankind toward a disaster, which will be
far more destructive than anything the world has seen so far, simply because it will
affect every single person living on this planet".
Bhatt's film makes a mockery of Government of India's claim of not allowing import of
any GM foods in the country as it conclusively demonstrates that supermarkets in India are
flooded with harmful food stuff and biotech MNCs are cashing on the ignorance of
unsuspecting consumers in India. "Indians are unfortunately kept in dark, and the
corporations are hatching strategies to cash in on their ignorance. Poison on the Platter
is, therefore, an attempt to generate awareness among consumers and kick start an informed
debate on the issue", said Bhatt.
Diet for a Dead Planet
Interview with Christopher Cook author of "Diet for a Dead Planet: How the Food
Industry is Killing Us"
Authors@Google: Marion Nestle
Nutritionist and Author Marion Nestle discusses her latest book, "What to
Eat" as well as her previous books "Food Politics: How the Food Industry
Influences Nutrition" and "Health and Safe Food: Bacteria, Biotechnology, and
Bioterrorism" as part of the Authors@Google series. A professor of nutrition at NYU,
Nestle was featured in the film "Super Size Me" and has been called "one of
the nation's smartest and most influential authorities on nutrition and food policy."
Authors@Google: David Kessler
David Kessler visits Google's Mountain View, CA headquarters to discuss his book
"The End of Overeating." This event took place on May 28, 2009, as part of the
Authors@Google series.
Before we can begin to address America's eating epidemic, we need to understand WHY we
have such difficulty controlling what we eat. Kessler spent the past seven years meeting
with top scientists, physicians, psychologists, and food industry insiders, and conducting
his own research to reveal how specific foods produced by giant food corporations and
restaurant chains ("Big Food") feed our desire to eat by stimulating the brain
with an infinite variety of diabolical combinations of salt, fat and sugar. People of all
ages are being set up for a lifetime of food obsession due to the ever-present
availability of foods laden with salt, fat and sugar. It is no wonder that millions of
Americans are gaining weight and getting sick. The End of Overeating provides a highly
readable and indispensable picture of the problems we face and offers solutions for how to
fight them and regain control.
David Kessler, MD, served as commissioner of the US Food and Drug Administration. Dr.
Kessler, a pediatrician, has been dean of the medical schools at Yale and the UCSF. He is
the father of two grown children and lives with his wife in California.
New Class of Compounds Discovered
for Potential Alzheimer’s Disease Drug, Penn Study Finds
A new class of molecules capable of blocking the formation of specific protein clumps that
are believed to contribute to the dementia of Alzheimer’s disease (AD) patients has
been discovered by researchers at the University of Pennsylvania School of Medicine. By
assaying close to 300,000 compounds, they have identified drug-like inhibitors of AD tau
protein clumping, as reported in the journal Biochemistry. Co-authors Alex Crowe, Research
Specialist; Kurt R. Brunden, PhD, Director of Drug Discovery at Penn’s Center for
Neurodegenerative Disease Research (CNDR); Virginia M.-Y. Lee, PhD, and John Q.
Trojanowski, MD, PhD, CNDR Co-Directors, and colleagues conducted the screen to find small
molecules that prevent the formation of the tau protein fibrils. These fibrils, a hallmark
pathological feature of AD, have been a holy grail for investigators hoping to better
treat AD and related neurodegenerative diseases.
Avian influenza strain primes brain
for Parkinson's disease
At least one strain of the H5N1 avian influenza virus leaves survivors at significantly
increased risk for Parkinson's disease and possibly other neurological problems later in
life, according to new research from St. Jude Children's Research Hospital. In the August
10 online early edition of the Proceedings of the National Academy of Sciences,
researchers reported that mice which survived infection with an H5N1 flu strain were more
likely than uninfected mice to develop brain changes associated with neurological
disorders like Parkinson's and Alzheimer's diseases. Parkinson's and Alzheimer's involve
lss of brain cells crucial to a variety of tasks, including movement, memory and
intellectual functioning. The study revealed the H5N1 flu strain caused a 17 percent loss
of the same neurons lost in Parkinson's as well as accumulation in certain brain cells of
a protein implicated in both diseases. "This avian flu strain does not directly cause
Parkinson's disease, but it does make you more susceptible," said Richard Smeyne,
Ph.D., associate member in St. Jude Developmental Neurobiology. Smeyne is the paper's
senior author. "Around age 40, people start to get a decline in brain cells. Most
people die before they lose enough neurons to get Parkinson's. But we believe this H5N1
infection changes the curve. It makes the brain more sensitive to another hit, possibly
involving other environmental toxins," Smeyne explained. Smeyne noted the work
involved a single strain of the H5N1 flu virus, the A/Vietnam/1203/04 strain. The threat
posed by other viruses, including the current H1N1 pandemic flu virus, is still being
studied. Early indications are that the H1N1 pandemic strain carries a low neurologic
risk, said Richard Webby, Ph.D., director of the World Health Organization Collaborating
Center for Studies on the Ecology of Influenza in Animals and Birds, which is based at St.
Jude. Webby, who is also an associate member of the St. Jude Department of Infectious
Diseases, was not involved in the H5N1 study led by Smeyne. This study also supports the
theory that a hit-and-run mechanism is at work in Parkinson's disease. The investigators
believe the H5N1 infection sparks an immune response that persists long after the initial
threat is gone, setting patients up for further devastating losses from a second hit,
possibly from another infection, drug or environmental toxin. In this case, researchers
believe the flu virus is the first hit that sets up development of Parkinson's at a later
time.
Certain behavioral traits and
feeding practices may increase risk for weight gain in children
Many clinicians and public health officials view parental involvement as an essential part
of solving the current childhood obesity epidemic. However, it's important for parents to
use the right approach when trying to combat childhood obesity. Restrictive feeding
practices, or forbidding certain foods, may not always be the best solution. A child's
inhibitory control, a behavior similar to self-control, may be more important than
parental restrictions. An article and related editorial soon to be published in The
Journal of Pediatrics, explore the relationship between a child's low inhibitory control,
parental restrictive feeding practices, and childhood weight gain. Stephanie Anzman, MS,
and Leann Birch, PhD, of the Center for Childhood Obesity Research at Pennsylvania State
University studied 197 non-Hispanic white girls. They collected information from the girls
and their parents over a 10-year period, beginning when the girls were 5 years old. In
addition to recording their body mass index (BMI), the researchers asked the girls whether
their parents restricted or forbade certain foods. The researchers also recorded the
parents' BMI, income, and education level. Additionally, mothers were asked to describe
their child's level of self-control. Anzman and Birch found that girls with lower
self-control had higher BMIs and gained more weight than those girls who demonstrated
better self-regulation. Girls with lower self-control were almost twice as likely to be
overweight by the age of 15. The authors also noticed a relationship between a child's
perception of parental restrictive feeding practices and weight gain. In other words, the
combination of high parental restriction and low self-control put girls at the highest
risk for weight gain among the group studied. According to Ms. Anzman, "Parental
attempts to help children with lower self-control by restricting their access to favorite
snack foods can make the forbidden foods more attractive, thereby exacerbating the
problem." She suggests that parents can help their children learn to control their
eating habits by allowing them to choose between healthy options. She adds that it is
often better to not keep restricted foods in the house. "That way," she
explains, "it is not necessary to constantly tell children they cannot have the foods
they want."
New light-emitting biomaterial
could improve tumor imaging, study shows
A new material developed at the University of Virginia – an oxygen nanosensor that
couples a light-emitting dye with a biopolymer – simplifies the imaging of
oxygen-deficient regions of tumors. Such tumors are associated with increased cancer
aggressiveness and are particularly difficult to treat. Oxygen nanosensors are powerful
new research tools that one day may also be used for the diagnosis and detection of
diseases and for planning treatment strategies. The new material is based on poly(lactic
acid), a biorenewable, biodegradable polymer that is safe for the body and the
environment, and is easy and inexpensive to fabricate in many forms, including films,
fibers and nanoparticles. It is useful for medical research as well as environmental
research, sustainable design and green products, too. The versatile sensor material is the
result of research combining green chemistry with nanotechnology, and is reported in the
current online edition of the journal Nature Materials. Chemists at the University of
Virginia developed the material and consulted with cancer researchers at the U.Va. Cancer
Center and Duke University Medical Center to determine possible applications. Guoqing
Zhang, a U.Va. chemistry doctoral candidate, working with Cassandra Fraser, a U.Va.
chemistry professor, synthesized the new material by combining a corn-based biopolymer
with a dye that is both fluorescent and phosphorescent. The phosphorescence appears as a
long-lived afterglow that is only evident under low oxygen or oxygen-free conditions.
Zhang devised a method to adjust the relative intensities of short-lived blue fluorescence
and long-lived yellow phosphorescence, ultimately creating a calibrated colorful glow that
allows visualization of even minute levels of oxygen. The biomaterial displays its
oxygen-sensitive phosphorescence at room or body temperature, making it ideal for use in
tissues. "We were amazed at how easy the material was to synthesize and fabricate as
films and nanoparticles, and how useful it is for measuring low oxygen
concentrations," Fraser said.
U.Va. Researchers Unlocking the
Healing Promise of Stem Cells Derived from Fat
Fat may carry negative connotations in today's world, but the stem cells found in fat
tissue may prove valuable for their potential to heal wounds. As Shayn Peirce-Cottler, an
assistant professor of biomedical engineering at the University of Virginia, describes
them, they are hard-working and tough. Although these adult stem cells lack the infinite
plasticity of embryonic stem cells, they can be used for therapeutic purposes without
raising the ethical issues that have made stem cell research so controversial. And, as
Peirce-Cottler has found in the course of a series of collaborations with Dr. Adam Katz,
an associate professor of plastic surgery, their healing powers are considerable.Fat stem
cells, known as adipose stromal cells, are easily separated from fat tissue after
liposuction. An advantage of liposuction is that it is much less invasive than the process
used for harvesting stem cells from bone marrow, the most prized source of adult stem
cells. Adipose stromal cells are also more plentiful than bone marrow stem cells, and they
are better able to tolerate harsh environments. This last quality is particularly
important. From a medical point of view, it means that adipose stromal cells can be
applied under conditions that would destroy other cells. In preclinical studies, Katz and
Peirce-Cottler have used them successfully to treat chronic diabetic ulcers, open sores
characterized by low levels of oxygen and high levels of bacteria. "In these
circumstances, they produce a sufficient quantity of growth factors so that the
wound-healing response is virtually normal," Peirce-Cottler said.
U of Minnesota researchers discover
high levels of estrogens in some industrial wastewater
In a groundbreaking study, civil engineering researchers in the University of Minnesota's
Institute of Technology have discovered that certain industries may be a significant
source of plant-based estrogens, called phytoestrogens, in surface water. They also
revealed that some of these phytoestrogens can be removed through standard wastewater
treatment, but in some cases, the compounds remain at levels that may be damaging to fish.
Civil engineering associate professor Paige Novak and her graduate student researcher Mark
Lundgren studied wastewater streams from 19 different industrial sites in Minnesota and
Iowa and analyzed them for six phytoestrogens. They found very high concentrations of
these hormone-mimicking phytoestrogens -- up to 250 times higher than the level at which
feminization of fish has been seen in other research -- in the wastewater discharged from
eight industrial sites, including biodiesel plants, a soy milk factory, a barbecue meat
processing facility and a dairy. They also detected high concentrations of phytoestrogens
in the water discharged by some municipal wastewater treatment plants. The good news is
that the researchers revealed that phytoestrogens can be removed from water as it goes
through standard treatment. In fact, they saw more than 90 percent removal of these
compounds from the water. Unfortunately, sometimes 99 percent removal is needed to reach
levels that are considered harmless to fish. Plant-based phytoestrogens are naturally
occurring but have been shown to function as hormone mimics and alter development and
reproductive patterns in fish. These effects include decreased aggression,
immunosuppression, and decreased testosterone production. Other estrogens that cause
similar effects have been linked to population-level collapse in fish, Novak said.
Life and death in the living brain
Like clockwork, brain regions in many songbird species expand and shrink seasonally in
response to hormones. Now, for the first time, University of Washington neurobiologists
have interrupted this natural "annual remodeling" of the brain and have shown
that there is a direct link between the death of old neurons and their replacement by
newly born ones in a living vertebrate. The scientists introduced a chemical into one side
of sparrow brains in an area that helps control singing behavior to halt apoptosis, a cell
suicide program. Twenty days after introduction of the hormones the researchers found that
there were 48 percent fewer new neurons than there were in the side of the brain that did
not receive the cell suicide inhibitor. "This is the first demonstration that if you
decrease apoptosis you also decrease the number of new brain cells in a live animal. The
next step is to understand this process at the molecular level," said Eliot
Brenowitz, a UW professor of psychology and biology and co-author of a new study. His
co-author is Christopher Thompson, who earned his doctorate at the UW and is now at the
Free University of Berlin. "The seasonal hormonal drop in birds may mimic what is an
age-related drop in human hormone levels. Here we have a bird model that is natural and
maybe similar genes have a similar function in humans with degenerative diseases such as
Alzheimer's and Parkinson's, as well as strokes, which are associated with neuron
death." The research involved Gambel's white-crowned sparrows, a songbird subspecies
that winters in California and migrates to Alaska in the spring and summer to breed and
raise its young. The sparrow's brain regions, including one called the HVC, which control
learned song behavior in males, expand and shrink seasonally. Thompson and Brenowitz
previously found that neurons in the HVC begin dying within four days hours after the
steroid hormone testosterone is withdrawn from the bird's brains. Thousands of neurons
died over this time.
A gene that may play a role in type
1 diabetes
Scientists at Stanford University have identified a gene that may play a role in the
development of type 1 diabetes, an autoimmune disease in which the immune system attacks
the body's insulin-producing cells. Insulin, a hormone produced by cells of the pancreas,
helps the body to absorb sugars found in food and to maintain blood sugar at appropriate
levels. The study team, led by C. Garrison Fathman, M.D., examined genes from mice that
develop a type 1 diabetes-like disease. Dr. Fathman is a grantee of the National Institute
of Allergy and Infectious Diseases and the National Institute of Diabetes and Digestive
and Kidney Diseases, both components of the National Institutes of Health. Additional
funding for the study was provided by the Special Statutory Funding Program for Type 1
Diabetes Research, a special appropriation for research on the prevention and cure for
type 1 diabetes. The investigators found that cells in the pancreatic lymph nodes of mice
make two forms of the same gene called deformed epidermal autoregulatory factor 1 (Deaf1).
One form is full-length and functional and the other is a shorter, nonfunctional variant
form. The full-length, functional form of Deaf1 controls the production of molecules
needed to eliminate immune cells that can destroy insulin-producing cells. The presence of
the Deaf1 variant was found to prevent the full-length Deaf1 protein from functioning
normally. Further experiments showed that the variant form blocked the genes needed to
produce certain molecules involved in immune regulation. When the researchers measured the
levels of these two forms in people with type 1 diabetes and in healthy individuals,
levels of the variant form were found to be higher in people with type 1 diabetes compared
with those in healthy controls. In addition, the variant form, as in mice, inhibited the
full-length form from functioning normally.
Misuse of common antibiotic is
creating resistant TB
Use of a common antibiotic may be undercutting its utility as a first-line defense against
drug-resistant tuberculosis (TB). Fluoroquinolones are the most commonly prescribed class
of antibiotics in the U.S. and are used to fight a number of different infections such as
sinusitis and pneumonia. They are also an effective first line of defense against TB
infections that show drug resistance. New research shows, however, that widespread general
use of fluoroquinolones may be creating a strain of fluoroquinolone-resistant TB. The
results are published in the August 15 issue of the American Thoracic Society's American
Journal of Respiratory and Critical Care Medicine. "While fluoroquinolone resistance
in TB strains has been reported since the mid 1990's, to our knowledge no one had
investigated the direct causes of it," said Dr. We wanted to determine whether and to
what extent clinical practices were having an effect of creating that resistance,"
said Rose A. Devasia, M.D., M.P.H., clinical instructor of Vanderbilt University. To
investigate the causes of the small but growing proportion of fluoroquinolone-resistant TB
cases, Dr. Devasia and colleagues performed a retrospective case-control study using data
from the Tennessee Department of Health. They analyzed the records of every newly
diagnosed patient with culture-confirmed TB who was also enrolled in Tennessee's Medicaid
program, TennCare between January 2002 and December 2006. Using the TennCare pharmacy
database, they were able to obtain information on the patients' use of fluoroquinolone for
the 12 months prior to their TB diagnosis. They used M. tuberculosis isolates taken from
each patient to test for fluoroquinolone resistance in each case. After excluding those
who were not enrolled in TennCare or whose culture were either unavailable or unusable,
the researchers analyzed data for 640 patients. Age, race and other demographic factors
were not significantly associated with resistance, but when researchers further analyzed
the data they found a linear association between previous fluoroquinolone exposure and
fluoroquinolone resistance. Overall, patients who had used fluoroquinolones within 12
months of diagnosis were almost five times as likely to have a fluoroquinolone-resistant
strain of TB than those who had not used fluoroquinolones, and there was a linear
association between length of fluoroquinolone use and fluoroquinolone resistance.
Predictors of disease behavior
change in Crohn’s disease
Using the Vienna classification system, it has been shown in clinic-based cohorts that
there can be a significant change in disease behavior over time, whereas disease location
remains relatively stable. Clinical and environmental factors as well as medical therapy
might be relevant in predicting disease behavior change in patients with CD. In previous
studies, early age at diagnosis, disease location, perianal disease and, in some studies,
smoking were associated with the presence of complicated disease and surgery. The combined
effect of markers of disease phenotype (e.g., age, gender, location, perianal diesease)
and medical therapy (steroid use, early immunosupression) on the probability of disease
behavior change were, however, not studied thus far in the published literature. A
research article to be published on July 28, 2009 in the World Journal of Gastroenterology
addresses this question. Members of the Hungarian IBD Study Group led by Dr Peter Laszlo
Lakatos from the Semmelweis University investigated 340 well-characterized, unrelated,
consecutive CD patients (M/F: 155/185, duration: 9.4 ± 7.5 years) with a complete
clinical follow-up. Medical records including disease phenotype according to the Montreal
classification, extraintestinal manifestations, use of medications and surgical events
were analyzed retrospectively. Patients were interviewed on their smoking habits at the
time of diagnosis and during the regular follow-up visits.
Metabolic bone disease in cirrhosis
patients
Long-standing liver disease has long been recognized to result in fragile bones with
increased risk of fractures. In various international studies, the overall incidence has
varied from 11% to 48%, with a fracture rate of 3%-44%. However, the reason for this is
poorly understood. With liver transplantation becoming a viable option in liver disease
and offering complete cure and long-term survival, bone disease is becoming the major
determinant of survival and quality of life in these patients. A research article to be
published on July 28, 2009 in the World Journal of Gastroenterology addresses this
question. This research team was led by Tushar R Bandgar from KEM Hospital, India. They
found that low bone formation and increased resorption led to fragile bones in these
patients. Contributing factors identified were inadequate sunlight exposure, reduced
physical activity, low body weight, vitamin D deficiency and low level of testosterone.
They also demonstrated that the severity of bone loss was accelerated in patients with low
IGF-1 level. IGF-1 is normally synthesized in the liver and its synthesis is affected
early in cirrhosis. The present study also found that the increased estrogen level seen in
cirrhosis was protective against osteopenia. These results shed new light on bone
disorders seen in patients with cirrhosis. As most of the factors identified are
correctable or treatable, it should provide additional help in treatment of these
patients, such that they have better quality of life and survival.
Characteristic pathological
findings in reflux esophagitis
Recently, the number of patients with GERD has increased in Japan. However, there have
been few reports about the pathological findings in the esophageal squamous epithelium,
and there are differing opinions among pathologists about the findings considered
characteristic of chronic reflux esophagitis.? Dr. Daisuke Asaoka and his colleagues from
Juntendo University (Japan) used a rat model of chronic acid-reflux esophagitis to explore
the esophageal mucosal damage macroscopically and microscopically throughout the entire
esophagus, including the upper esophagus close to the hypopharynx, and to investigate the
protective effects of ecabet sodium (ES) on the esophageal mucosa. This will be published
on July 28, 2009 in the World Journal of Gastroenterology, Their research revealed that
epithelial thickening occurs at the same time as inflammatory cell infiltration in the
middle to lower esophagus in chronic acid-reflux esophagitis. Furthermore, they
demonstrated that inflammatory cells infiltrated the epithelium of the upper esophagus
close to the hypopharynx, where there was no evidence of ulcers. These findings suggested
that the reflux of gastric juice can extend to the upper esophagus close to the
hypopharynx. Moreove, the research also demonstrated that ES inhibited the epithelial
thickening of the lower and middle esophagus, which suggested that ES may play a useful
defensive role in the prevention of reflux esophagitis.
Chinese acupuncture affects brain's
ability to regulate pain, UM study shows
Acupuncture has been used in East-Asian medicine for thousands of years to treat pain,
possibly by activating the body's natural painkillers. But how it works at the cellular
level is largely unknown. Using brain imaging, a University of Michigan study is the first
to provide evidence that traditional Chinese acupuncture affects the brain's long-term
ability to regulate pain. The results appear online ahead of print in the September
Journal of NeuroImage. In the study, researchers at the U-M Chronic Pain and Fatigue
Research Center showed acupuncture increased the binding availability of mu-opoid
receptors (MOR) in regions of the brain that process and dampen pain signals –
specifically the cingulate, insula, caudate, thalamus and amygdala. Opioid painkillers,
such as morphine, codeine and other medications, are thought to work by binding to these
opioid receptors in the brain and spinal cord. "The increased binding availability of
these receptors was associated with reductions in pain," says Richard E. Harris,
Ph.D., researcher at the U-M Chronic Pain and Fatigue Research Center and a research
assistant professor of anesthesiology at the U-M Medical School. One implication of this
research is that patients with chronic pain treated with acupuncture might be more
responsive to opioid medications since the receptors seem to have more binding
availability, Harris says. These findings could spur a new direction in the field of
acupuncture research following recent controversy over large studies showing that sham
acupuncture is as effective as real acupuncture in reducing chronic pain.
An HIV-blocking gel for women
University of Utah scientists developed a new kind of "molecular condom" to
protect women from AIDS in Africa and other impoverished areas. Before sex, women would
insert a vaginal gel that turns semisolid in the presence of semen, trapping AIDS virus
particles in a microscopic mesh so they can't infect vaginal cells. "The first step
in the complicated process of HIV (human immunodeficiency virus) infection in a woman is
the virus diffusing from semen to vaginal tissue. We want to stop that first step,"
says Patrick Kiser, an associate professor of bioengineering at the University of Utah's
College of Engineering. "We have created the first vaginal gel designed to prevent
movement of the AIDS virus. This is unique. There's nothing like it." "We did it
to develop technologies that can enable women to protect themselves against HIV without
approval of their partner," he adds. "This is important – particularly in
resource-poor areas of the world like sub-Sahara Africa and south Asia where, in some age
groups, as many as 60 percent of women already are infected with HIV. In these places,
women often are not empowered to force their partners to wear a condom." A study
testing the behavior of the new gel and showing how it traps AIDS-causing HIV particles
will be published online later this week in the journal Advanced Functional Materials.
Kiser is the senior author. "Due to cultural and socioeconomic factors, women often
are unable to negotiate the use of protection with their partner," says Julie Jay,
the study's first author and a University of Utah doctoral candidate in pharmaceutics and
pharmaceutical chemistry.
Tumor suppressor pulls double shift
as reprogramming watchdog
A collaborative study by researchers at the Salk Institute for Biological Studies
uncovered that the tumor suppressor p53, which made its name as "guardian of the
genome", not only stops cells that could become cancerous in their tracks but also
controls somatic cell reprogramming.Although scientists have learned how to reprogram
adult human cells such as skin cells into so-called induced pluripotent stem cells
(iPSCs), the reprogramming efficiency is still woefully low. The Salk study, published in
the Aug. 9 advance online edition of Nature, gives new insight why only a few cells out of
many can be persuaded to turn back the clock. "Although we have been able to
reprogram specialized cells for a while now, there had been nothing known about the
control mechanisms that prevent it from happening spontaneously in the body and why it has
been so hard to change their fate in a Petri dish," says Juan-Carlos Izpisúa
Belmonte, Ph.D., a professors in the Gene Expression Laboratory, who worked closely with
Geoffrey M. Wahl, Ph.D., also a professor in the Gene Expression Laboratory. Their
findings bring iPSCs technology a step closer to fulfilling its promise as source of
patient-specific stem cells but also force scientists to rethink the development of
cancer. "There's been a decade-old idea that cancer arises through the
de-differentiation of fully committed and specialized cells but eventually it was
discarded in favor of the currently fashionable cancer stem cell theory," says Wahl.
"Now, that we know that p53 prevents de-differentiation, I believe it is time to
reconsider the possibility that reprogramming plays a role in the development of cancer
since virtually all cancer cells lose p53 function in one way or another." As
mammalian embryos transition through a series of developmental stages, the choices of
embryonic stem cells, which enjoy almost limitless prospects, are progressively limited
till they eventually give rise to the roughly 200 cell types that make up our body and
generally lack the ability to revert back to a less specialized stage. Although
differentiation is generally irreversible, scientists have developed several methods to
overcome the cells' reluctance to be reprogrammed. The most widely used technology
involves the forced expression of four transcription factors—Oct4, Sox2, Klf4, and
c-Myc—in fully committed adult cells.
More insulin-producing cells, at
the flip of a 'switch'
Researchers have found a way in mice to convert another type of pancreas cell into the
critical insulin-producing beta cells that are lost in those with type I diabetes. The
secret ingredient is a single transcription factor, according to the report in the August
7th issue of Cell, a Cell Press journal. Then the gene called Pax4 is forced on in
pancreatic alpha cells, the cells change their identity to become beta cells, the
researchers found. The body in turn senses a loss of alpha cells, replaces them with new
alpha cells and then converts those too into beta cells. The hope is that a treatment
based on the findings in mice might find its way to human patients, although "a lot
of ifs remain before we will know whether it could be taken to the clinic," said
Patrick Collombat of Inserm in France. For instance, it's not yet known whether the
findings in mice will translate to human tissue. Even if they do, scientists would need to
find a way to turn Pax4 on and then back off again once a sufficient number of beta cells
were in place. Still, the findings hold considerable promise. "The strategy we use is
a good one," said Ahmed Mansouri of the Max-Planck Institute for Biophysical
Chemistry in Germany. "It's a new idea that we might use one factor. Normally, we
would have thought it would take more." The results also show that the pancreas is in
general capable of such regeneration. "It shows there are progenitors [in the
pancreas] that can be activated," Mansouri said.
Wistar scientists find key to
strengthening immune response to chronic infection
A team of researchers from The Wistar Institute has identified a protein that could serve
as a target for reprogramming immune system cells exhausted by exposure to chronic viral
infection into more effective "soldiers" against certain viruses like HIV,
hepatitis C, and hepatitis B, as well as some cancers, such as melanoma. Effective
response by key immune cells in the body, called T cells, is crucial for control of many
widespread chronic viral infections such as HIV and hepatitis B and C. Virus-specific CD8
T cells, also known as "killer" T cells, often lose their ability to control
viral replication and become less effective over time, a process known as T cell
exhaustion. Understanding how optimal antiviral T cell responses are suppressed in these
circumstances is crucial to developing strategies to prevent and treat such persisting
infections. In the August 6 on-line issue of Immunity, the research team led by Wistar
assistant professor E. John Wherry, Ph.D., describes how the protein Blimp-1
(B-lymphocyte-induced maturation protein 1) represses the normal differentiation of CD8 T
cells into memory T cells, which recognize disease-causing agents from previous infections
and enable the body to mount faster, stronger immune responses. The team also reports that
Blimp-1 causes exhausted CD8 T cells to express inhibitory receptors, which prevent
recognition of specific antigens, further weakening immune response. The researchers
describe how complete deletion of Blimp-1, which is overexpressed in CD8 T cells during
chronic viral infection, reversed these aspects of T cell exhaustion. By identifying
Blimp-1 as a transcription factor associated with T cell exhaustion the findings open the
window for reprogramming exhausted killer T cells back into prime infection-fighting form.
"We are very excited by the identification of Blimp-1 as a key transcriptional
regulator of T cell exhaustion," says senior author Wherry. "Transcription
factors like Blimp-1 are key molecules involved in global control of cell fate and
differentiation, and Blimp-1 in particular prevents cells from de-differentiating or
re-differentiating.
Sensitizing tumor response to
cancer therapy
Two forms of skin and brain cancer respond very poorly to chemotherapy and radiation:
melanoma and glioblastoma multiforme brain cancer. Both are the focus of an intensive
effort in the department of nutritional sciences at The University of Arizona to find
natural, biologically active compounds that will sensitize the cancerous tumors to therapy
without damaging normal tissue. By using the compounds in conjunction with conventional
treatment, the researchers hope patient survival rates will ultimately increase. The
incidence of melanoma, an aggressive and often fatal form of skin cancer, is increasing at
the rate of 3 percent annually, according to the American Cancer Society. Dacarbazine, the
standard chemotherapeutic drug for melanoma for decades, has been ineffective when used
alone. To improve its performance, Randy Burd, assistant professor of nutritional sciences
and member of the UA's BIO5 Institute, has been testing the drug and its new analog
Temozolomide in combination with various bioactive compounds to gain greater response
rates on melanoma tumors in cell cultures. "After working with COX-2 inhibitors
– which had complications – we started looking at quinones, which occur in
nature as pigments, vitamin biochemical backbones and plant compounds, and then we
analyzed the enzymes involved in their activation," Burd said. Quercetin, a
polyphenol found in apples, onions, green tea and other plant-based foods, is a quinone
that has shown an interesting effect on melanoma tumors. In low concentrations quercetin
behaves as an antioxidant, yet at high concentrations it becomes a cell-damaging
pro-oxidant. Burd's group is exploiting the pro-oxidant attribute of quercetin, using
tyrosinase, which is the highly expressed enzyme responsible for the pigment formation in
human skin cells that grow out of control in melanoma. "The quercetin is similar to
precursors of melanin," Burd said. "The tyrosinase actually recognizes and
activates quercetin to a pro-oxidant rather than an antioxidant." When tested
together in melanoma tumor cell cultures, the result is tumor cell death. The melanoma
enzyme is tricked into activating so much quercetin that it turns around and sensitizes
the melanoma cells to the chemotherapy drug, and they die.
Johns Hopkins researchers make stem
cells from developing sperm
The promise of stem cell therapy may lie in uncovering how adult cells revert back into a
primordial, stem cell state, whose fate is yet to be determined. Now, cell scientists at
the Johns Hopkins University School of Medicine have identified key molecular players
responsible for this reversion in fruit fly sperm cells. Reporting online this week in
Cell Stem Cell, researchers show that two proteins are responsible redirecting cells on
the way to becoming sperm back to stem cells. "We knew from our previous work that
cells destined to be sperm could revert back to being stem cells, but we didn't know
how," says Erika Matunis, Ph.D., an associate professor of cell biology at the Johns
Hopkins University School of Medicine. "Since, dedifferentiation is an interesting
phenomenon probably occurring in a lot of different stem cell populations, we wanted to
know more about the process." Like all stem cells, each of the nine stem cells in the
fly testis divides to form two daughter cells: One stays a stem cell and the other
differentiates into an adult cell, in this case, a sperm cell. To figure out what might
cause sperm cells to revert or dedifferentiate, Matunis's research team genetically
altered the flies so that both cells become sperm, reducing the stem cell population in
the testis to nothing.About a week later, the team examined these fly testes and found
that the stem cells had been repopulated.
Genomic signature in blood
identifies underlying viral infection
Scientists have identified a genomic "signature" in circulating blood that
reveals exposure to common upper respiratory viruses, like the cold or flu, even before
symptoms appear. The tell-tale viral signature reflects a set of subtle but robust changes
in genes that are activated as the body responds to infection. The signal from the
signature is strong enough in symptomatic individuals to clearly reveal whether their
infection is viral or bacterial. It can also discriminate between who has a viral
infection and who does not - all from a single tube of blood. "This work is still in
a relatively early phase of discovery, but we are optimistic that these findings may lead
to a whole new way of diagnosing infectious disease," says Geoffrey Ginsburg, M.D.,
Ph.D., director of Duke University's Center for Genomic Medicine in the Institute for
Genome Sciences & Policy and the senior author of the study appearing in the journal
Cell Host & Microbe. Researchers say the discovery could lead to dramatic changes in
the way doctors care for the millions of people who develop upper respiratory infections
every year. Ginsburg says the symptoms of a cold, the flu or pneumonia can appear similar,
but right now, doctors can't tell what the patient really has until laboratory tests are
conducted, and that can take days. "Until results are in, treatment is pretty much a
best guess. Knowing exactly which pathogen is involved is important because it affects the
urgency of response and the type of treatment," says Ginsburg. "This approach
could lead to more precise, informed and tailored therapy – essentially, personalized
care for infectious disease. That's better for the patient and better for public health,
in general." Christopher Woods, M.D., an associate professor of medicine at Duke and
the Chief of the Infectious Disease Section at the Durham Veterans Administration Medical
Center, says a quick test to determine the real cause of disease has other benefits, too.
"It could mean more appropriate use of antibiotics. Overuse of antibiotics can lead
to the emergence of drug-resistant pathogens, and no one wants to see more of that."
The discovery is based upon the fact that the body's immune system starts responding very
quickly and in a highly specific manner when exposed to a viral pathogen as opposed to a
bacterial one. "A detailed reading of that response, using gene expression data,
reveals what type of pathogen the person is reacting to," says Aimee Zaas, M.D.,
M.H.S., an infectious diseases physician at Duke and the lead author of the study.
Study links selection for
pathogen-resistance with increased risk for inflammatory disease
New research reveals that a simple laboratory assay detects a genetic variation in host
response to bacterial infection that is associated with an increased susceptibility for
inflammatory disease. The study, published by Cell Press online on August 6th in the
American Journal of Human Genetics, also provides fascinating insight into the link
between evolution and the ability to ward off pathogens. "While previous genome-wide
association studies and scans for selection have identified genes important for human
disease, there is a growing need for approaches that provide mechanistic information for
how variants impact disease pathogenesis and to identify genetic variation in traits
subject to natural selection," explains senior study author Dr. Samuel Miller from
the University of Washington in Seattle. Dr. Miller and colleagues used a novel screen of
bacterial infection to identify human variation in Salmonella-induced cell death. "By
examining variation in human cell-based measures of infectious disease susceptibility and
severity, we can begin to link variation affecting human disease and variation identified
as being the subject of natural selection," explains lead author Dr. Dennis Ko. The
researchers observed that a more robust host response to Salmonella was associated with
nonfunctional CARD8, a gene thought to be a key negative regulator of inflammation. A
comparison of CARD8 genes among different mammalian populations suggested that the
increase in infectious disease burden associated with animals that live in herds or
colonies may have naturally selected for loss of CARD8 multiple times in mammalian
evolution. A similar process may have occurred in humans, as the authors also showed that
loss of function of CARD8 is more common among populations that adopted agriculture
earlier, while it is less common in populations that have traditionally lived as
hunter-gatherers. The researchers hypothesized that loss of CARD8 may be one way in which
a population evolves a more robust host response to deal with infectious diseases.
Positive expectations help patients
recover from whiplash 3 times faster
Positive thoughts bring positive things to people and it's well documented these
expectations have helped people recover from a number of health conditions. But until now,
not much was known about the correlation between that belief and the recovery from
injuries like whiplash. Two University of Alberta researchers and a colleague from Sweden
have found some answers to that question in three different studies on expectations for
recovery. Linda Carroll, in the School of Public Health, looked at a cohort of over 6,000
adults with traffic-related whiplash injuries. She found that those that had positive
outlooks towards their recovery actually recovered over three times faster than those who
did not. Dejan Ozegovic, also in the School of Public Health, looked at predications
around returning to work, using the same cohort. Positive return-to-work assumptions meant
people rated themselves as "recovered" 42 per cent faster than those who had
more negative expectations.Lena Holm, a Swedish researcher who is working at the U of A
this summer, found that those study participants in Sweden who had low expectations of
complete recovery were four times more likely to still feel symptoms of the injury six
months later. The researchers were surprised by the findings, which showed that the
severity of the injury did not have an impact on the recovery times.
Gene shut-down may offer early
warning of chronic leukemia
A new study shows that certain genes are turned off early, before clinical signs of the
disease appear, in the development of chronic leukemia. The study, led by researchers at
the Ohio State University Comprehensive Cancer Center - James Cancer Hospital and Solove
Research Institute, examined cancer cells from patients with chronic lymphocytic leukemia
(CLL) and from a new strain of mice that develops a very similar disease. The findings
suggest that changes called epigenetic alterations, which silence a gene's ability to make
its protein, might serve as markers for detecting CLL early and for monitoring its
progression. They also point to a strategy for treating the disease earlier using drugs
that reverse such changes, and further confirm the value of the mouse model for studying
CLL causes and treatment, researchers say. The research revealed that a gene called FOXD3
likely plays a key role in CLL, and that the gene is silenced early, followed by the
silencing of other genes. The findings are published online in the Proceedings of the
National Academy of Sciences Early Edition. "Our data suggest that the silencing of
FOXD3 might represent a very early gene involved in the initiation of CLL that we can
potentially target for re-expression with specific drugs," says study leader Dr. John
C. Byrd, professor of internal medicine, director of the hematologic malignancies program
at the James Cancer Hospital and Solove Research Institute and a CLL specialist.
"Next, we need to learn whether therapy to reverse this silencing can delay or
prevent CLL progression." An estimated 15,500 Americans are expected to develop CLL
in 2009, and about 4,400 people will die of the disease. The malignancy usually strikes
people aged 50 or older, causing white blood cells called B lymphocytes to proliferate.
This can lead to severe anemia and dangerous viral, bacterial and fungal infections.
Average survival is eight to 12 years from diagnosis.
Bringing solar power to the masses
On a 104-degree Friday in July when sunlight bathed The University of Arizona campus,
doctoral student Dio Placencia sat before a noisy vacuum chamber in the Chemical Sciences
Building trying to advance the renewable energy revolution. As a member of UA professor
Neal R. Armstrong's research group, Placencia conducts research aimed at creating a thin,
flexible organic solar cell that could power a tent or keep a car charged between trips to
work and back home again. He's passionate about renewable energy and says it's a waste
that so little solar has been incorporated into society. "I have a little flat panel
that I walk around with," Placencia said. "I usually put that on my backpack,
and I charge my cell phone when I'm walking to school." The sun is clean and free.
"Here it is," he said. "Why not use it?" Across the University,
professors, researchers, students and others involved in policy planning and economic
analysis are working to make that question moot. In a region noted for abundant sunlight,
they are chipping away at problems like how to employ solar at the utility-generating
plant level, how to harness it to charge the newly indispensable products of the day
– cell phones, MP3 players, laptops – what to do at night and when clouds halt
the energy giveaway from the sky. The research proceeds in labs amid state-of-the-art
equipment funded by multimillion-dollar federal grants. It's the product of students'
hunches and long careers spent unlocking the mysteries of science. Along the way, students
are being immersed in a nascent industry that many hope will be the economic engine of the
next decade. "Looking at renewable energy is a perfect place to emphasize that we
don't know where the next breakthrough is going to be," said Leslie P. Tolbert, UA
vice president for research, graduate studies and economic development. "Somewhere in
a lab someplace, there's somebody figuring out a whole new way to capture sunlight. In
fact, there are many people doing that. And even they are depending on knowing that there
is, behind them, a cadre of basic science researchers producing new information that will
feed their thoughts." Armstrong, a professor of chemistry and optical sciences at the
UA, occasionally teaches freshman chemistry. He decided one day near the end of the
semester to try to make the material even more relevant. "I said to myself, well,
lithium ion batteries in my cell phone, in my iPod," – his daughter had given
him one – "I wonder how much coal we burn to charge those guys up at the end of
the day. Because that's one of the big drivers for portable power, to get all this stuff
off the grid." After making some very conservative calculations, he arrived at an
answer, which he shared with the class: "You burn about a quarter of a pound of coal
per charge of your lithium ion battery, and you generate about half a pound of CO2 per
charge, per battery, per day .... The room got really quiet."
Curcumin May be Viable Supplement
to Treat Inflammatory Bowel Disease
Turmeric – the key ingredient in curry – has been used in India for thousands of
years to help treat colds, inflammation, arthritis and even cancer. Now, researchers at
the Steele Children's Research Center at The University of Arizona have found that
curcumin (the biologically active ingredient in turmeric) may be a viable supplement to
treat inflammatory bowel disease, known as IBD.Basically, they have shown that curcumin
decreases the severe inflammation and resultant intestinal damage caused by IBD. IBD
refers to two inflammatory diseases: Crohn's disease, which affects the entire
gastrointestinal tract, and ulcerative colitis, which affects the colon. Both cause severe
abdominal pain, diarrhea, vomiting, fatigue and weight loss. As many as one in 500
individuals will be diagnosed with IBD each year, and IBD typically is diagnosed in
children and young adults between the ages of 10 and 19. Approximately 1 million
individuals in the United States suffer from IBD. For several years, Steele Children's
Research Center researchers have been investigating how curcumin aids in treating IBD.
Recently, Steele Center principal investigator Pawel Kiela, research associate professor,
and co-investigator Dr. Fayez K. Ghishan, MD, Steele Center director and professor, and
their team made some new discoveries regarding how curcumin may be used as a supplemental
treatment for IBD.
An overview of global dimming and
brightening
Radiation from the Sun fuels life on Earth and determines the climate of its inhabitants.
The amount of radiation that reaches the Earth's surface helps to control evaporation
rates, snow and glacier melt, carbon uptake through plant photosynthesis, the severity of
seasons, and agricultural productivity. Thus changes in the amount of solar energy
reaching the Earth can affect society, the environment, and the economy. A growing body of
evidence supports that human interference has affected the amount of solar radiation that
is able to penetrate the atmosphere—in general, aerosol pollutants have been shown to
scatter or absorb incoming solar radiation and increase the reflectance and lifetime of
clouds, thereby reducing the amount of solar radiation reaching the Earth's surface.
Dubbed "global dimming," this phenomenon has been countered in the past few
decades by "global brightening" as pollution control efforts have met with
success. Wild reviews the evidence surrounding global dimming and brightening, addressing
a number of frequently asked questions such as how and when dimming and brightening
originated, how dimming and brightening affects other global environmental processes,
whether current climate models successfully replicate observed patterns in dimming and
brightening, and how dimming and brightening may evolve over the coming decades.
Brain difference in psychopaths
identified
Professor Declan Murphy and colleagues Dr Michael Craig and Dr Marco Catani from the
Institute of Psychiatry at King’s College London have found differences in the brain
which may provide a biological explanation for psychopathy. The results of their study are
outlined in the paper 'Altered connections on the road to psychopathy', published in
'Molecular Psychiatry'. The research investigated the brain biology of psychopaths with
convictions that included attempted murder, manslaughter, multiple rape with strangulation
and false imprisonment. Using a powerful imaging technique (DT-MRI) the researchers have
highlighted biological differences in the brain which may underpin these types of
behaviour and provide a more comprehensive understanding of criminal psychopathy. Dr
Michael Craig said ‘If replicated by larger studies the significance of these
findings cannot be overestimated. The suggestion of a clear structural deficit in the
brains of psychopaths has profound implications for clinicians, research scientists and
the criminal justice system.’ While psychopathy is strongly associated with serious
criminal behaviour (eg rape and murder) and repeat offending, the biological basis of
psychopathy remains poorly understood. Also some investigators stress mainly social
reasons to explain antisocial behaviours. To date, nobody has investigated the
'connectivity' between the specific brain regions implicated in psychopathy.
