News 23 juli 2009
Daily potassium citrate wards off
kidney stones in seizure patients on high-fat diet
Children on the high-fat ketogenic diet to control epileptic seizures can prevent the
excruciatingly painful kidney stones that the diet can sometimes cause if they take a
daily supplement of potassium citrate the day they start the diet, according to research
from Johns Hopkins Children's Center. A report on the work is published in the August
issue of Pediatrics. "We can confidently say this is a safe and powerful way to
prevent kidney stones, and it should become part of standard therapy in all ketogenic
dieters, not just those who already show elevated urine calcium levels," says senior
investigator Eric Kossoff, M.D., a pediatric neurologist at Hopkins Children's. "If
you wait, it might be too late." The ketogenic diet, believed to work by initiating
biochemical changes that eliminate seizure-triggering short circuits in the brain's
signaling system, is given to many children whose seizures do not respond to medications.
But the diet, which consists of high-fat foods with very few carbohydrates, causes a
buildup of calcium in the urine and the formation of kidney stones in about 6 percent of
those on it. Hopkins Children's adopted the preventive treatment with potassium citrate
two years ago, and doctors now believe this one major side effect of the diet is a thing
of the past, allowing more children to remain on the diet for longer. Potassium citrate
taken twice daily, either as powder sprinkled on food or dissolved in water, is believed
to inhibit stone formation.
Purer water made possible by Sandia
advance
By substituting a single atom in a molecule widely used to purify water, researchers at
Sandia National Laboratories have created a far more effective decontaminant with a shelf
life superior to products currently on the market. Sandia has applied for a patent on the
material, which removes bacterial, viral and other organic and inorganic contaminants from
river water destined for human consumption, and from wastewater treatment plants prior to
returning water to the environment. “Human consumption of ‘challenged’
water is increasing worldwide as preferred supplies become more scarce,” said Sandia
principal investigator May Nyman. “Technological advances like this may help solve
problems faced by water treatment facilities in both developed and developing countries.
”The study was published in June 2009 in the journal Environmental Science &
Technology (a publication of the American Chemical Society) and highlighted in the June 22
edition of Chemical & Engineering News. Sandia is working with a major producer of
water treatment chemicals to explore the commercial potential of the compound.
Researchers Identify Genes Linked
to Chemoresistance
Two genes may contribute to chemotherapy resistance in drugs like 5-fluorouracil, which is
used in liver cancer treatment, according to Virginia Commonwealth University Massey
Cancer Center researchers. Liver cancer is a highly aggressive form that has limited
therapeutic options. One of the key challenges with cancer treatment is that patients can
develop resistance to chemotherapy. Researchers are examining ways to prevent resistance
by determining the molecular mechanisms involved with cancer progression, and then
developing new generations of chemotherapeutic agents. In the study, published online in
the Early Edition of the Proceedings of the National Academy of Sciences the week of July
13, researchers reported that two genes - astrocyte elevated gene-1, or AEG-1, and late
SV40 factor, LSF, contribute to resistance of a commonly used chemotherapeutic drug called
5-fluorouracil, or 5-FU. The team found that over-expression of AEG-1 increased resistance
of the liver cells to 5-FU. They observed that a second gene, LSF, is under the control of
AEG-1 and mediates a series of molecular pathways involved the resistance to 5-FU.
Starve a Fever, Feed a Cold, Don't
Be Stressed
Whether it's getting a cold during exam time or feeling run-down after a big meeting,
we've all experienced feeling sick following a particularly stressful time at work or
school. Is this merely coincidence, or is it possible that stress can actually make us
sick? In a new report in Perspectives on Psychological Science, a journal of the
Association for Psychological Science, psychologist Janice K. Kiecolt-Glaser from the Ohio
State University College of Medicine reviews research investigating how stress can wreak
havoc on our bodies and provides some suggestions to further our understanding of this
connection. The field of psychoneuroimmunology (PNI) investigates how stress and negative
emotions (such as depression and anxiety) affect our health. Over the past 30 years,
researchers in this field have uncovered a number of ways that stress adversely affects
our health, and specifically, how stress can damage our immune system. Numerous studies
have shown that stressed individuals show weaker immune responses to vaccines, and as
Kiecolt-Glaser observes, "The evidence that stress and distress impair vaccine
responses has obvious public health relevance because infectious diseases can be so
deadly." Stress and depression have been shown to increase the risk of getting
infections and also result in delayed wound healing. Inflammation is the body's way of
removing harmful stimuli and also starts the process of healing, via release of a variety
of chemicals known as proinflammatory cytokines (e.g., interleukin-6). However, too much
inflammation can be damaging and has been implicated in the development of many
age-related diseases, including Alzheimer's Disease, Parkinson's disease, arthritis, and
Type II diabetes. Negative emotions and psychological stressors increase the production of
proinflammatory cytokines. A recent study revealed that men and women who serve as
caregivers to spouses with dementia (and thus are under constant stress) have a four times
larger annual rate of increase in serum interleukin-6 levels compared to individuals
without caregiving responsibilities.
University of Minnesota research
leads to new technology to protect human health
Larry Wackett and Michael Sadowsky, members of the University of Minnesota’s
BioTechnology Institute, developed an enzyme that is used in Bioo Scientific’s new
MaxDiscovery™ Melamine Test kit, which simplifies the detection of melamine
contamination in food. Melamine is an industrial chemical that killed six Chinese children
and hospitalized 150,000 last year after it was added to milk to increase its apparent
protein content. Some children may have life-long chronic kidney problems resulting from
melamine exposure. Development of the test responds to a call from the World Health
Organization (WHO) for a simple, inexpensive method to detect melamine contamination in
infant formula and other liquids. Until now, melamine testing required expensive
laboratory equipment and skilled personnel. This kit simplifies the testing and reduces
the cost of melamine detection. The MaxDiscovery Melamine Test kit can detect melamine in
milk, powdered milk, cream, ice cream and chocolate drink. Bioo Scientific has plans to
adapt it to detect melamine in seafood and meat. Researchers at the BioTechnology
Institute (BTI) developed the enzyme, melamine deaminase, used in the MaxDiscovery
Melamine Test kit and the enzyme will be produced in the BTI Pilot Plant fermentation
facilities. Melamine deaminase works by breaking one of the C-N bonds in melamine to
release ammonia, which can be detected by a simple test that turns the liquid blue.
Jennifer Seffernick, a research associate in Wackett’s lab, discovered the enzyme
while conducting research on biodegradation of s-triazine herbicides. It is one of many
examples of how basic research can lead to new technologies that benefit society.
"Development of the melamine enzyme and the test kit is an example of how
universities and industry can collaborate to foster basic science, education, and
technology that benefits society," says Wackett, who is a Distinguished McKnight
University Professor in the College of Biological Sciences.
Review provides new insights into
the causes of anorexia
New imaging technology provides insight into abnormalities in the brain circuitry of
patients with anorexia nervosa (commonly known as anorexia) that may contribute to the
puzzling symptoms found in people with the eating disorder. In a review paper published on
line in Nature Reviews Neuroscience, Walter Kaye, MD, professor of psychiatry and director
of the Eating Disorders Program at the University of California, San Diego, and colleagues
describe dysfunction in certain neural circuits of the brain which may help explain why
people develop anorexia in the first place, and behaviors such as the relentless pursuit
of dieting and weight loss. "Currently, we don't have very effective means of
treating people with anorexia," said Kaye. "Consequently, many patients with the
disorder remain ill for years or eventually die from the disease, which has the highest
death rate of any psychiatric disorder." A better understanding of the underlying
neurobiology – how behavior is coded in the brain and contributes to anorexia
—is likely to result in more effective treatments, according to the researchers.
Childhood personality and temperament may increase an individual's vulnerability to
developing anorexia. Predisposing factors, some suspected to be inherited, such as
perfectionism, anxiety, or obsessive-compulsive tendencies may precede the onset of an
eating disorders. These traits become intensified during adolescence as a consequence of
many factors such as hormonal changes, stress and culture. "Adolescence is a time of
transition, when individuals must learn to balance immediate and long-term needs and goals
in order to achieve independence," said Kaye. "For such individuals, learning to
cope with mixed societal messages and pressures may be overwhelming, exacerbating
underlying traits of anxiety and a desire to perfectly achieve." Once a patient
develops anorexia, starvation and malnutrition cause profound effects on the brain and
other organ systems. Such changes include neuro-chemical imbalances, which may, in turn,
exaggerate the preexisting traits and accelerate the disease process.
Mayo Clinic researchers find first
potential pathogenic mutation for restless legs syndrome
An international team of researchers led by scientists at the Mayo Clinic campus in
Florida have found what they believe is the first mutated gene linked to restless legs
syndrome, a common neurologic disorder. The researchers, who reported the findings in the
July 21 issue of Neurology, doubt that a large proportion of the millions of people who
suffer from the syndrome have this mutated MEIS1 gene. They point out, however, that
understanding the function of both the normal and abnormal genes will shed some insights
into this mysterious disorder. Restless legs syndrome affects between 5 and 11 percent of
the population in Europe and in North America. The condition is characterized by
unpleasant sensations in the legs at rest, especially in the evening, that are temporarily
relieved by movement. Because restless legs syndrome often interrupts sleep, people
commonly are diagnosed after they consult a sleep specialist for assistance. "We
think restless legs syndrome may be due to a number of clinical factors, but we also
believe that there is a strong genetic component to the disorder," says the study's
lead investigator, Carles Vilariño-Güell, Ph.D., a neuroscientist at Mayo Clinic,
Jacksonville. "The mutation we found is in a portion of the protein that is identical
in species as distinct to human as frogs and fish, which tells us that this portion is
very important for the proper function of the protein and that the mutation has a very
high chance of causing disease," he says. While common variants (different versions)
of MEIS1 and BTBD9, another associated gene, have been found in families with a high
incidence of restless legs syndrome, it is not clear that those variants are capable of
causing disease, Dr. Vilariño-Güell says. "This mutation, on the other hand, is the
first that we think can be a real candidate for causing or promoting restless legs
syndrome," he says.
Screening for childhood depressive
symptoms could start in second grade
New research indicates that screening children for symptoms of depression, the most common
mental health disorder in the United States, can begin a lot earlier than previously
thought, as early as the second grade.A University of Washington study that followed
nearly 1,000 children from the second to the eighth grades also found five distinct
patterns for the way symptoms of depression develop among adolescents. "Some children
are reporting that they don't have as many friends, feel lonelier and are more anxious
than their peers," said James Mazza, a UW professor of educational psychology and
lead author of the study. "They are telling us that they feel different from the
typical happy- go-lucky second grader. "We can start to build a profile of children's
mental health in the second grade. This is important because children who are experiencing
depression symptoms early on may be at great risk for mental health concerns during
adolescence, based on other research studies. We want to reassure parents that everyone,
including children, may feel sad or depressed once in a while, but that doesn't mean they
will go on to develop depression. We are trying to understand how depression starts and
evolves in childhood so that we can develop interventions to help children," Mazza
said.The new study relied on annual self reports from the children as well as parental and
teacher evaluations collected as part of the Raising Healthy Children study, a larger,
long-term investigation looking at the development of healthy and problem behaviors among
children at 10 suburban schools in the Pacific Northwest. The depression study used data
from 511 boys and 440 girls, and 81 percent of the participants were white. The study
identified five patterns of depression symptoms, but 56 percent of the children showed no
or very few symptoms of depression in the second grade.
Genetic marker linked to problem
behaviors in adults with developmental disabilities
A common variation of the gene involved in regulating serotonin and norepinephrine in the
brain may be linked to problem behaviors in adults with developmental and intellectual
disabilities, new research indicates. The findings were published in the July 2009 issue
of the American Journal on Intellectual and Developmental Disabilities and are available
online at http://tinyurl.com/mw8baj. "Problem behaviors in these populations account
for billions of dollars in intervention costs each year, but nearly all of these
interventions occur after the fact," Craig Kennedy, a co-author of the study and
professor of special education at Vanderbilt University's Peabody College of education and
human development, said. "This research suggests one way we might predict which
individuals are at risk of being aggressive and destructive and provide treatment before
problems occur." Fifteen to 20 percent of adults with developmental/intellectual
disabilities have problem behaviors. For this study, the researchers focused specifically
on aggression, self-injury or property destruction and set out to determine if there was a
genetic underpinning for these behaviors. They focused on the gene that encodes monoamine
oxidize A or MAOA. MAOA is involved in the regulation of the neurotransmitter serotonin,
which is linked to appetite and mood, and the neurotransmitter and hormone norepinephrine,
which is linked to the fight-or-flight response. Previous studies found that variations in
MAOA were linked to violent behavior. "We found that a common variant of the MAOA
gene was strongly associated with problem behaviors in adults with developmental and / or
intellectual disabilities," Kennedy said. The researchers studied 105 white men
between the ages of 18 and 50. The individuals were divided into three groups: those with
developmental/intellectual disabilities and a history of more than 10 years of problem
behavior, those with the disabilities but without problem behavior, and a typically
developing control group. Only white men were sampled because the MAOA gene is linked to
the X chromosome and also is shown to vary by ethnicity. Forty-three percent of those with
developmental/intellectual disabilities and behavior problems had the gene variant,
compared to 20 percent of the same group with no behavior issues and 20 percent of a
typically developing control group.
A genetic basis for schizophrenia
Schizophrenia is a severely debilitating psychiatric disease that is thought to have its
roots in the development of the nervous system; however, major breakthroughs linking its
genetics to diagnosis, prognosis and treatment are still unrealized. Jill Morris, PhD
assistant professor of Pediatrics at Northwestern University's Feinberg School of Medicine
and a researcher in the Human Molecular Genetics Program of Children's Memorial Research
Center studies a gene that is involved in susceptibility to schizophrenia, Disc1
(Disrupted-In-Schizophrenia 1). Two recent publications by Morris and colleagues focus on
the role of Disc1 in development, particularly the migration of cells to their proper
location in the brain and subsequent differentiation into their intended fate. During
development, cells need to properly migrate to their final destination in order to develop
into the appropriate cell-type, integrate into the corresponding network of cells and
function properly. Disruption of cell migration can lead to inappropriate cell development
and function, resulting in disease. The first paper, published in the July 2009 online
issue of the journal Development, followed the role of Disc1 in cranial neural crest (CNC)
cells, which are multi-potent cells that give rise to multiple cell types including
craniofacial cartilage and the peripheral nervous system during development. They also are
similar to neurons in their high mobility, response to signals and cellular origin. The
Morris laboratory determined that Disc1 regulates two stem cell maintenance factors that
have many functions in CNC cells, including the maintenance of precursor pools, timing of
migration onset and the induction of cell differentiation. The authors showed that Disc1
disruption results in increased expression of these factors, leading to hindered cell
migration and a change in cell fate. "This research indicates that Disc1 may be
involved in regulating stem cells and their fate," says Morris. The second paper,
published in the June 2009 online issue of Human Molecular Genetics, studied the
hippocampus, a brain area that is involved in learning and memory, and is also associated
with the pathology of schizophrenia. Disc1 is highly expressed in the hippocampus,
particularly the dentate gyrus, which is considered the gateway to the hippocampus. In
this study, the authors decreased Disc1 expression using RNA interference in the
developing mouse hippocampus. The loss of Disc1 resulted in hindered migration of dentate
gyrus granule cells to their proper location in the brain. "Improper migration of
hippocampal neurons may result in altered connectivity in the brain," says Morris.
New research finds possible genetic
link to cause of pregnancy loss and disorders
Scientists at the University of Tennessee, Knoxville, and Lawrence Berkeley National
Laboratory (LBNL) have published new findings about a cause of a condition at the root of
genetic disorders such as Down Syndrome, pregnancy loss and infertility.Called aneuploidy,
the condition is an abnormal number of chromosomes, and the research team found that if a
mother's egg cell has a mutation in just one copy of a gene, called Bub1, then she is less
likely to have offspring that survive to birth. The findings appear in the online early
edition of the Proceedings of the National Academy of Sciences for the week of July 13.
Sundar Venkatachalam, an assistant professor of biochemistry and cellular and molecular
biology at UT Knoxville, originally was studying the gene for a possible connection to
colon cancer, when he found his lab mice showed strange fertility characteristics.
"Where you would normally expect a female to have eight to 10 pups, there were only
one or two pups that survived to term in the litters of females that had one copy of
Bub1," said Venkatachalam. "So this was unusual when we were looking for cancer
effects, especially in this group of females." Ordinarily, both copies of a gene in a
chromosome must carry the same mutation in order for an organism to be adversely effected,
but the drastic effects of a single mutation were unexpected. Venkatachalam, working with
pathologist Robert Donnell at the UT College of Veterinary Medicine and LBNL researcher
Francesco Marchetti, also found that the harmful effects of this mutation increased with a
mother's age. As the female mice got older, there was eventually a complete loss of their
ability to support a full-term pregnancy that lined up with an increase in aneuploidy. The
same is true in humans: the chance of having an aneuploid pregnancy increases with the age
of the mother. For the past several years, scientists have used mice to study the genetic
causes of aneuploidy. They've zeroed in on mutations in a handful of genes as the
culprits, including Bub1.
Rates of secondhand smoke exposure
high among college students
Secondhand smoke (SHS) is not only a nuisance, but a potential health concern for many
college students, and administrators should be taking steps to reduce students' exposure,
according to a new study by researchers at Wake Forest University School of Medicine.It is
the first study to provide evidence of the high rates of SHS exposure, and correlates of
exposure, among college students in the United States. Funded by the National Institute on
Alcohol Abuse and Alcoholism, the study can be found online today and will appear in the
July 23 issue of Nicotine & Tobacco Research, a publication of the Society for
Research on Nicotine and Tobacco. "It is well-known that there are some serious
health issues surrounding secondhand smoke," said Mark Wolfson, Ph.D., lead author on
the study, professor and section head for the Section on Society and Health in the
Department of Social Sciences and Health Policy. "While some college campuses are
smoke free, others have virtually no restrictions on smoking, not even in the residence
halls. There is a growing national movement to move away from that, but it still very much
varies by campus. In this first study to evaluate SHS exposure among college students, we
were really kind of floored to see how many, and how frequently, students are exposed to
it." For the study, researchers surveyed 4,223 undergraduate college students from 10
North Carolina universities – eight public and two private. They were asked questions
about their drinking and smoking habits, demographics (age, gender, race, parents'
education level), lifestyle (residence on- or off-campus, living in a substance-free
dormitory, participation in a fraternity or sorority) and SHS exposure. Of the
participants, 83 percent reported having been exposed to SHS at least once in the seven
days preceding the survey. Most of those exposures (65 percent) happened at a restaurant
or bar, followed by exposure at home or in the same room as a smoker (55 percent) and in a
car (38 percent). Daily and occasional smokers were more likely than nonsmokers to report
exposure, perhaps not surprising given that they are more likely than other students to
have friends who smoke and to frequent or live in locations where smoking occurs,
according to the study. Similarly, students who binge drink were more likely than other
students to report exposure to SHS, likely reflective of the co-occurrence of smoking and
drinking among college students. Other factors that appeared to be associated with
increased exposure to SHS included living in residence locations where smoking is allowed
or locations associated with smoking, such as Greek houses and off-campus housing, being
female, of white race, having parents with higher education levels and attending a public
versus private school. Nearly all nonsmokers (93.9 percent) and the majority of smokers
(57.8 percent) reported that SHS was somewhat or very annoying.
Are we what our mothers ate?
The time between ovulation and conception may be a critical one for maternal and fetal
health, according to Kelle Moley, M.D., Washington University School of Medicine. In mouse
studies, she found that subtle differences in maternal metabolism had long-lasting
effects. Indeed, when Dr. Moley transferred embryos from a diabetic mouse into a
non-diabetic mouse shortly after egg implantation, she noted neural tube defects, heart
defects, limb deformities and growth defects in offspring. These findings indicate that we
may need to re-direct our ideas about maternal health to the time prior to pregnancy, she
says.
1 gene that contributes to breast
cancer's aggressive behavior identified
Aggressive forms of cancer are often driven by the abnormal over-expression of
cancer-promoting genes, also known as oncogenes. Studies at the Genome Institute of
Singapore (GIS), a research institute under the Agency for Science, Technology and
Research (A*STAR) of Singapore, have identified a gene, known as RCP (or RAB11FIP1), that
is frequently amplified and over-expressed in breast cancer and functionally contributes
to aggressive breast cancer behaviour.The research findings are published in the July 20th
online issue of Journal of Clinical Investigation (JCI). The GIS team, led by Lance
Miller, Ph.D., and Bing Lim, Ph.D., initially discovered that RCP expression was
positively correlated with cancer recurrence in a population of breast cancer patients.
This suggested that RCP may be required by some tumours for growth and metastatic spread
to other organs. When the researchers over-expressed RCP in non-cancerous breast cells,
they found that RCP promotes migration, or cellular movement, which is a precursor to the
ability of tumours to invade neighbouring tissues.
EU and Canada settle WTO case on
Genetically Modified Organisms
The European Union and Canada have today
signed in Geneva a final settlement of the WTO dispute that Canada brought against the EU
in May 2003 regarding the application of its legislation on biotech products. The mutually
agreed solution provides for the establishment of a regular dialogue on issues of mutual
interest on agriculture biotechnology. The EU and Canada will notify this settlement to
the WTO Dispute Settlement Body as a mutually agreed solution. EU Trade Commissioner
Ashton said: "The mutually agreed solution with Canada is a clear sign that this type
of dialogue works. I hope we can follow the same constructive approach with Argentina and
the United States." EC regulatory procedures on genetically modified organisms are
working normally, as evidenced by 21 authorisations since the date of establishment of the
WTO panel. The European Commission has held regular discussions on biotech-related issues
with the three complainants in this case – Canada, Argentina and the United States -
since the adoption of the WTO panel report in 2006. The settlement reached with Canada
provides for bi-annual meetings between competent services of the European Commission and
Canadian authorities on agricultural biotechnology market access issues of mutual
interest, including:
* GM product approvals in the territory of
Canada or the EU as well as, where appropriate, forthcoming applications of commercial
interest to either side.
*The commercial and economic outlook for future approvals of genetically modified
products.
*Any trade impact related to asynchronous approvals of genetically modified products or
the accidental release of unauthorised products, and any appropriate measures in this
respect.
*Any biotech-related measures that may affect trade between Canada and the EU, including
measures of EU Member States.
*Any new legislation in the field of agriculture biotechnology.
*Best practices in the implementation of legislation on biotechnology
This dialogue is aimed at an exchange of
information that would contribute to avoiding unnecessary obstacles to trade. The EU is
not expected to modify its current regulatory regime on biotech products, which was never
subject to WTO challenge in itself. Following a complaint by the US, Canada and Argentina
against the EU on the application of its legislation on biotech products, the WTO Dispute
Settlement Body (DSB) adopted on 21 November 2006 three panel reports which found a
violation of the WTO Sanitary and Phytosanitary (SPS) Agreement on three grounds:
* The application of a general de facto
moratorium on approval of GM products from June 1999 to August 2003
*The existence of undue delays with respect to 23 product-specific applications (out of
the 27 cases considered by the Panel).
*National safeguard measures introduced by 6 Member States before the establishment of the
panel, which were found not to be based on an appropriate risk assessment.
Subsequently, the EU and the three
complainants (US, Argentina and Canada) agreed to engage in technical discussions on
biotech-related issues, which would not be limited to issues of implementation of the WTO
panel recommendations. The EU and the complainants also reached an agreement for a
12-month Reasonable Period of Time for implementation (i.e. until 21 November 2007). The
complainants agreed to further extend the RPT until 11 January 2008, where they would take
stock of progress and decide the way forward.
The complainants have taken different
positions in view of the expiration of that extended RPT:
(a) Argentina and Canada have agreed to
several extensions of the RPT, most recently until 31 December 2009 and 31 July 2009 July,
respectively. Technical discussions with Argentina and Canada have continued to date.
(b) The US made a general retaliation
request on 17 January 2008. On 6 February 2008, the EU objected to the US retaliation
request. The matter was referred to arbitration under Article 22.6 of the Dispute
Settlement Understanding at the special meeting of the DSB held on 8 February 2008. On 15
February 2008, and according to the sequencing agreement concluded between the US and the
EU, both parties requested the suspension of Article 22.6 procedures. The chairman of the
arbitration panel suspended those procedures on 18 February 2008. Those procedures can
only be resumed following the examination of compliance of the panel report by the EU
through an arbitration procedure under Article 21.5 of the Dispute Settlement
Understanding (DSU). The US and the EU continued technical discussions in 2008. The last
round of discussions took place in October 2008.
For more on dispute settlement at the WTO
see
http://ec.europa.eu/trade/issues/respectrules/dispute/index_en.htm
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