News 10 april 2009
Researchers find promotion is bad
for mental health and stops you visiting the doctor
New research by economics and psychology
researchers at the University of Warwick has found that promotion on average produces 10%
more mental strain and gives up to 20% less time to visit the Doctors. In a research paper
entitled “Do People Become Healthier after Being Promoted” Chris Boyce and
Professor Andrew Oswald of the University of Warwick questioned why people with higher job
status seem to have better health. A long-held assumption by researchers is that an
imprvement to a person’s job status, through a promotion, will directly result in
better health due to an increased sense of life control and self-worth.
The researchers tested this. They drew upon the British Household Panel Survey data set,
collected annually between 1991 and 2005, with information on approximately 1000
individual promotions. They found no evidence of improved physical health after promotion
– nor that self-assessed feelings of health declined.
Genes from tiny marine algae
suggest unsuspected avenues for new research
By sequencing the DNA of two tiny marine
algae, a team of scientists has opened up a myriad of possibilities for new research in
algal physiology, plant biology, and marine ecology. The project was led by Alexandra
Worden at the Monterey Bay Aquarium Research Institute (MBARI) and the Joint Genome
Institute (JGI). The genome analyses involved a collaborative effort between MBARI, JGI,
and an international consortium of scientists from multiple institutions, including
University of Washington, Ghent University (Belgium), and Washington University in St.
Louis. Initial discoveries from the research appear in the April 10, 2009 edition of
Science magazine. Biologists generally agree that all land plants, from tiny mosses to
giant redwoods, evolved from an ancestral green alga. Some of the closest representatives
of these ancestral green algae living today are thought to be the Prasinophytes, a group
of microscopic green algae found across the world's oceans. Microbial oceanographer
Alexandra Worden led a team of scientists that sequenced the genomes of two Prasinophytes
in the genus Micromonas. Each Micromonas cell is only about one fiftieth the width of a
human hair. However, they are widespread and may serve as important links in marine food
webs. They may also influence the amount of carbon dioxide the oceans take up from the
atmosphere. Worden's team spent four years compiling a complete list of the approximately
21 million chemical building blocks (called bases) that make up Micromonas' DNA. The
recent Science paper highlights key aspects of this genetic "Morse code." The
paper also compares Micromonas' genes with genes found in other organisms.
Study finds multidrug-resistant
gram-negative bacteria high in long-term care
The prevalence of a certain form of
drug-resistant bacteria, called multidrug-resistant gram-negative (MDRGN) organisms, far
surpassed that of two other common antimicrobial-resistant infections in long-term care
facilities, according to a study conducted by researchers at Hebrew SeniorLife's Institute
for Aging Research. Residents at long-term care facilities are one of the main reservoirs
of antimicrobial-resistant bacteria. Epidemiological studies have focused primarily on two
common antimicrobial-resistant organisms—methicillin-resistant Staphylococcus aureas
(MRSA) and vancomycin-resistant enterococci (VRE).
"Recently, it has become apparent that multidrug resistance among gram-negative
bacteria is becoming an even greater problem in these facilities, with nearly half of
long-term care facility residents harboring multidrug-resistant gram-negative
bacteria," write the researchers, led by IFAR's Erin'O'Fallon, M.D., M.P.H., in the
January issue of the Journal of Gerontology: Medical Sciences. MDRGN infection can lead to
toxins in the bloodstream that cause inflammation and destroy healthy tissue. Left
untreated, these infections can be fatal. More than 80 percent of the MDRGN cases in the
study were resistant to commonly prescribed antimicrobial medications, including
ciprofloxacin, trimethoprim-sulfamethoxazole, and amipicillin/sulbactam. By definition all
of the identified MDRGN bacteria were resistant to at least three different classes of
antimicrobial drugs, with one-third of them resistant to four.
Test quickly assesses whether
Alzheimer's drugs are hitting their target
A test developed by physician-scientists at
Washington University School of Medicine in St. Louis may help assess more quickly the
ability of Alzheimer's drugs to affect one of the possible underlying causes of
Alzheimer's disease in humans, accelerating the development of new treatments. Scientists
used the test to show that an Alzheimer's drug given to healthy volunteers reduced
production of a substance known as amyloid beta (A-beta), a normal byproduct of human
metabolism that builds to unhealthy levels forming brain plaques in Alzheimer's patients.
The drug candidate, LY450139, which is also known as semagacestat, is being studied in
clinical trials by Eli Lilly and Company.Ongoing clinical trials are studying the effect
that semagacestat may have on cognitive function and biochemical and brain imaging
biomarkers in patients with Alzheimer's disease. Washington University researchers wanted
to see whether the new measurement technique, stable isotope-linked kinetics (SILK), could
detect the study drug's impact on A-beta synthesis in healthy volunteers. "Bringing
an Alzheimer's disease drug into clinical trials from tests in animal models has always
been challenging," says study director Randall Bateman, M.D., a Washington University
neurologist who treats patients at Barnes-Jewish Hospital. "We haven't had a way to
quickly and accurately assess a drug's effects, and that meant there always had to be some
degree of educated guesswork when it came to setting the optimal dosage for humans. SILK
may help to eliminate much of that guesswork."
CSHL researchers explain process by
which cells 'hide' potentially dangerous DNA segments
The DNA in the 23 pairs of chromosomes in
each of the billions of cells of the human body is so tightly packed that it would measure
six feet in length if stretched end to end. A genome of this size can squeeze into a
cell's tiny nucleus because it is compressed into highly condensed chromatin fibers by
proteins called histones.All chromatin in the cell nucleus represents a massive
condensation of the genetic material. But a portion of it might well be called
super-condensed; it forms a kind of chromatin called heterochromatin. The genes contained
within these portions of the genome are effectively "silenced" because they
cannot be accessed by the cell's DNA-activating machinery. These "hidden" parts
of the genome also include highly repetitive, gene-poor, regions. Some of these, if
unpacked, would set loose DNA sequences that act like parasites – able to jump around
to other areas, sometimes randomly, unleashing genetic chaos.To assemble heterochromatin,
numerous molecules participate in an elaborate series of maneuvers that have gradually
come to light. "But scientists have been a little hazy on the initial steps and
requirements that get this process going," says Professor Leemor Joshua-Tor, Ph.D.,
of Cold Spring Harbor Laboratory (CSHL). She and her research team have now brought this
process into sharper focus by identifying a critical requirement for heterochromatin to be
established in the nucleus.In a report that appears online on April 9th in the journal
Molecular Cell, they show that the assembly of heterochromatin depends on the strength
with which a protein called Chp1 binds to a specific target site located on a histone
protein that has attached to the double helix.
Small RNAs can play critical roles
in male infertility/contraception
University of Nevada School of Medicine
scientists in the Department of Physiology and Cell Biology have discovered insight into
the reproductive workings of the male sex chromosome that may have significant
implications for male infertility and contraception. This important discovery has been
published in Nature Genetics, one of the highest-ranking journals in the field of
biomedical research based upon the impact factor.
The study findings indicate that the X chromosome in developing sperm cells encodes
numerous tiny ribonucleic acids called microRNAs despite the fact that that most of genes
on the X chromosomes are suppressed. This unprecedented observation implies that these
small RNAs have critical roles in chromosome inactivation and also in sperm formation.
"The sex chromosome silencing in meiotic male germ cells is a well-known phenomenon,
which has been termed meiotic sex chromosome inactivation. I was surprised when we first
observed that numerous microRNAs were highly expressed in these cells," said Wei Yan,
M.D., Ph.D., principal investigator for the study and associate professor of physiology
and cell biology at the School of Medicine. Working in collaboration with Dr. John
McCarrey, professor of molecular biology and reproductive biology at the University of
Texas, San Antonio, Yan's research group further investigated all the known X-linked
microRNAs. Their data confirm that these X chromosome-derived microRNAs indeed escape the
silencing effects and mange to be expressed. "This finding opens a new avenue towards
understanding the role of these small RNA species in the control of sperm production.
Worldwide, one in nine couples in their reproductive age experience infertility. On the
other hand, the number of unintended pregnancy is increasing yearly. Since these small
RNAs are involved in the control of sperm formation, they can be causative factors in male
infertility and also can be used as non-hormonal male contraceptive targets," added
Yan.
Scientists identify chemical
compound that may stop deadly brain tumors
Researchers at the University of North
Carolina at Chapel Hill School of Medicine have identified a compound that could be
modified to treat one of the most deadly types of cancer, and discovered how a particular
gene mutation contributes to tumor growth. The findings and potential treatment apply to a
type of brain tumor called secondary glioblastoma multiforme (GBM). GBMs are part of a
larger group of brain tumors called malignant gliomas, which is the type of cancer Senator
Edward Kennedy suffers from. A report of the research will appear in the April 10, 2009
issue of the journal Science. In experiments with tumor cells, the researchers reversed
the effects of a mutation in a gene called isocitrate dehydrogenase-1 (IDH1) by
replenishing a compound called ?-ketoglutarate (?-KG). "When the IDH1 gene is
mutated, the level of ?-KG is reduced, which in turn contributes to tumor growth by
helping to increase the supply of nutrients and oxygen to tumor cells. When we added the
?-KG to tumor cells, the effects caused by the IDH1 mutation were reversed," said Yue
Xiong, Ph.D., William R. Kenan Jr., Distinguished Professor of Biochemistry and Biophysics
and a member of the UNC Lineberger Comprehensive Cancer Center. "If scientists can
develop ?-KG into a clinical drug, it could potentially be used for treating brain tumor
patients who have this specific gene mutation. The ?-KG compound is already there; it only
needs to be modified to be used clinically, so that may save a lot of time," Xiong
said.
New therapeutic strategy could
target toxic protein in most patients with Huntington's disease
Howard Hughes Medical Institute researchers
have designed tiny RNA molecules that shut off the gene that causes Huntington's disease
without damaging that gene's healthy counterpart, which maintains the health and vitality
of neurons. Laboratory studies suggest that a single small interfering RNA could reduce
production of the damaging Huntingtin protein in nearly half of people with the disease.
Another 25 percent of patients might benefit from one of a set of four additional small
interfering RNAs. Phillip D. Zamore, an HHMI investigator at the University of
Massachusetts Medical School in Worcester, and his colleagues reported their findings in
an article published April 9, 2009, in the journal Current Biology. There is no treatment
for Huntington's disease, which is caused by a mutant form of the Huntingtin gene.
Huntingtin is required for healthy nerve cells, but the mutant gene makes a toxic protein
that contains excess amounts of the amino acid glutamine. The key to whether the
Huntingtin gene is normal or defective lies in a kind of genetic stutter: a repetitive
sequence of the DNA triplet CAG, which codes for the amino acid glutamine. Stretches of
CAG "repeats" appear in every human being's Huntingtin gene, but the length
varies. Whereas the normal gene has a sequence of between six and 34 CAG repeats, the
abnormal gene contains many more. In fact, any stretch of DNA containing more than 40 of
these repeats ensures that its bearer will develop Huntington's—the greater the
number of repeats, the earlier the disease strikes and the greater its ferocity. The
abnormal Huntingtin protein causes movement disorders, cognitive failure, and ultimately,
death. Children who have a parent with Huntington's disease have a 50 percent chance of
inheriting the disease themselves. Zamore studies how RNA interference can be used to
silence genes selectively. In the 1990s, he and other scientists learned they could shut
down the production of specific proteins by introducing double-stranded RNA into the cell
that is identical to the RNA they wanted to turn off. These strands of RNA, known as short
interfering RNA (siRNA), slice apart the original RNA, which the cell then destroys. But
nine years ago, when researcher Neil Aronin, who is also at UMass Medical School, proposed
using the technique to attack Huntington's, Zamore couldn't see a way. "I explained
to him that you can't," Zamore said. The problem was that the disease gene and its
healthy allele are almost identical, and Zamore told Aronin that he wouldn't be able to
distinguish between the two forms of Huntingtin. "Then, as he was leaving my office,
it occurred to me that you could," he recalled. The key was something called a single
nucleotide polymorphism or SNP.
Biological FM signal maintains
inflammation in cancer, asthma and other diseases
A study published tomorrow (10 April) in
Science examines a key player in conditions such as cancer, inflammatory bowel disease,
rheumatoid arthritis and asthma and has shown that cells use a sophisticated communication
system to coordinate responses to infection and maintain inflammation in the body. This
system is now a target for designing drugs to treat these conditions. Scientists funded by
the Biotechnology and Biological Sciences Research Council (BBSRC), the Medical Research
Council (MRC) and the Engineering and Physical Sciences Research Council (EPSRC) have
combined biological experiments and mathematics to discover the secrets of NF-kappaB
– a biological machine that coordinates the setting up and maintenance of
inflammation in the body by broadcasting a signal to surrounding cells. The team from the
Universities of Liverpool, Manchester and Warwick, along with scientists from
pharmaceutical company AstraZeneca (AstraZeneca R & D, Charnwood) have used Systems
biology – a multidisciplinary approach that uses a combination of experimental and
theoretical techniques to tackle biological problems – to investigate the role of
NF-kappaB. Professor Michael White of the University of Liverpool, who led the research
said: "We know that successive peaks and troughs in the amount of NF-kappaB –
forming a wave-like pattern over time – can exert exquisite control over many
biological processes that underlie the symptoms of inflammation. Furthermore, what we now
see is that different cell processes are determined once they pick up the frequency of
peaks and troughs in the NF-kappaB signal, just like tuning in to an FM radio
signal."
ISU researcher identifies protein
that concentrates carbon dioxide in algae
Increasing levels of carbon dioxide in the
atmosphere are a concern to many environmentalists who research global warming. The lack
of atmospheric carbon dioxide (CO2) concentration, however, actually limits the growth of
plants and their aquatic relatives, microalgae. For plants and microalgae, CO2 is vital to
growth. It fuels their photosynthesis process that, along with sunlight, manufactures
sugars required for growth.
CO2 is present in such a limiting concentration that microalgae and some plants have
evolved mechanisms to capture and concentrate CO2 in their cells to improve photosynthetic
efficiency and increase growth.
An Iowa State University researcher has now identified one of the key proteins in the
microalgae responsible for concentrating and moving that CO2 into cells.
Aerosols may drive a significant
portion of arctic warming
Though greenhouse gases are invariably at
the center of discussions about global climate change, new NASA research suggests that
much of the atmospheric warming observed in the Arctic since 1976 may be due to changes in
tiny airborne particles called aerosols. Emitted by natural and human sources, aerosols
can directly influence climate by reflecting or absorbing the sun's radiation. The small
particles also affect climate indirectly by seeding clouds and changing cloud properties,
such as reflectivity. A new study, led by climate scientist Drew Shindell of the NASA
Goddard Institute for Space Studies, New York, used a coupled ocean-atmosphere model to
investigate how sensitive different regional climates are to changes in levels of carbon
dioxide, ozone, and aerosols. The researchers found that the mid and high latitudes are
especially responsive to changes in the level of aerosols. Indeed, the model suggests
aerosols likely account for 45 percent or more of the warming that has occurred in the
Arctic during the last three decades. The results were published in the April issue of
Nature Geoscience. Though there are several varieties of aerosols, previous research has
shown that two types -- sulfates and black carbon -- play an especially critical role in
regulating climate change. Both are products of human activity. Sulfates, which come
primarily from the burning of coal and oil, scatter incoming solar radiation and have a
net cooling effect on climate. Over the past three decades, the United States and European
countries have passed a series of laws that have reduced sulfate emissions by 50 percent.
While improving air quality and aiding public health, the result has been less atmospheric
cooling from sulfates. At the same time, black carbon emissions have steadily risen,
largely because of increasing emissions from Asia. Black carbon -- small, soot-like
particles produced by industrial processes and the combustion of diesel and biofuels --
absorb incoming solar radiation and have a strong warming influence on the atmosphere.
Ancient diatoms lead to new
technology for solar energy
Engineers at Oregon State University have
discovered a way to use an ancient life form to create one of the newest technologies for
solar energy, in systems that may be surprisingly simple to build compared to existing
silicon-based solar cells.The secret; diatoms. These tiny, single-celled marine life forms
have existed for at least 100 million years and are the basis for much of the life in the
oceans, but they also have rigid shells that can be used to create order in a natural way
at the extraordinarily small level of nanotechnology. By using biology instead of
conventional semiconductor manufacturing approaches, researchers at OSU and Portland State
University have created a new way to make "dye-sensitized" solar cells, in which
photons bounce around like they were in a pinball machine, striking these dyes and
producing electricity. This technology may be slightly more expensive than some existing
approaches to make dye-sensitized solar cells, but can potentially triple the electrical
output. "Most existing solar cell technology is based on silicon and is nearing the
limits of what we may be able to accomplish with that," said Greg Rorrer, an OSU
professor of chemical engineering. "There's an enormous opportunity to develop
different types of solar energy technology, and it's likely that several forms will
ultimately all find uses, depending on the situation." Dye-sensitized technology, for
instance, uses environmentally benign materials and works well in lower light conditions.
And the new findings offer advances in manufacturing simplicity and efficiency.
"Dye-sensitized solar cells already exist," Rorrer said. "What's different
in our approach are the steps we take to make these devices, and the potential
improvements they offer." The new system is based on living diatoms, which are
extremely small, single-celled algae, which already have shells with the nanostructure
that is needed. They are allowed to settle on a transparent conductive glass surface, and
then the living organic material is removed, leaving behind the tiny skeletons of the
diatoms to form a template.
Babraham researchers reveal how
immune cells can be harnessed to target melanoma
Researchers at the Babraham Institute and
the University of Catanzaro "Magna Graecia", Italy, co-ordinating an
international network of scientists and clinicians from Europe, the USA and Japan, have
identified new mechanisms through which the immune system recognises and responds to
tumours like melanomas. This discovery may offer therapeutic approaches for tackling
metastatic melanoma, an aggressive form of skin cancer responsible for around 2,000 deaths
in the UK each year. These exciting new findings, published in the online edition of the
Journal of Clinical Investigation, reveal how a type of white blood cell - Natural Killer
(NK) cells - tackles tumours, characterising for the first time the molecular interactions
that lead to melanoma destruction. This has advanced understanding of melanoma recognition
by the immune system and has the potential to open up new avenues of research into the
prevention of metastasis by harnessing NK cells’ natural immunity. Natural Killer
cells are found in the blood, the lymph glands and in tissues such as the liver, the lungs
and the uterus, where they participate in immune defences against infection, cancer, in
reproductive success and in transplantation. They play a key role in the immune response
that targets tumour cells, while sparing healthy cells; mouse models revealed that NK
cells prevent and control tumour growth although, in the case of melanomas, the molecular
interactions behind this and how NK cells control metastatic progression had until now
remained elusive. The team of researchers, led by Francesco Colucci, Group Leader at the
Babraham Institute and Ennio Carbone, of the University of Catanzaro "Magna
Graecia", Italy, studied both human metastatic melanomas - aggressive forms of skin
cancer that have spread to other sites - and spontaneous mouse melanomas.
