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Week 40
Ultrasound can predict tumour
burden and survival in melanoma patients, sparing many people unnecessary surgery
Researchers have shown for the first time that patterns of ultrasound signals can be used
to identify whether or not cancer has started to spread in melanoma patients, and to what
extent. The discovery enables doctors to decide on how much surgery, if any, is required
and to predict the patient’s probable survival. Dr Christiane Voit told Europe’s
largest cancer congress, ECCO 15 – ESMO 34 [1], in Berlin today (Wednesday 23
September): “We have identified two ultrasound patterns of lymph node metastasis in
melanoma patients which can identify correctly any amount of tumour cells in the sentinel
lymph nodes in 75-90% of cases before proceeding to surgery on the sentinel lymph
nodes.” Dr Voit, who is a dermatologist and head of the diagnostic unit at the Skin
Cancer Centre at Charité – Universitätsmedizin Berlin, the Medical University of
Berlin, Germany, said that although her research needs to be confirmed in multi-centre,
randomised clinical trials, it had the potential to spare patients unnecessary surgery,
especially if it was combined with ultrasound-guided fine needle biopsy of lymph nodes
rather than conventional surgery.
Sorafenib significantly improves
the length of time before breast cancer worsens: results from first, large randomised
trial /
One of the first of a series of trials to investigate the use of sorafenib – a
targeted anti-cancer drug – for the treatment of advanced breast cancer has found
that if it is combined with the chemotherapy drug, capecitabine, it makes a significant
difference to the time women live without their disease worsening. Principal investigator
of the study, Professor José Baselga told Europe’s largest cancer congress, ECCO 15
– ESMO 34 [1], in Berlin today (Wednesday 23 September): “This is the first,
large, randomised study that demonstrates significant clinical activity of sorafenib in
breast cancer when given in combination with chemotherapy. Our results showed that
patients who received sorafenib plus capecitabine had a 74% percent improvement in the
time they lived without their disease worsening compared to those who received the
chemotherapy alone. This is a very positive study and the magnitude of the benefit is such
that it suggests that this agent will be an important addition to our therapeutic armoury
in breast cancer.” Sorafenib (Nexavar®) is a potent multi-kinase inhibitor, which
works by interfering with the growth of cancer cells and slowing the growth of new blood
vessels within the tumour. Until now, it has only been used in the treatment of kidney and
liver cancer.
New stove dramatically improves
lung health in Mexican women
Women in Central Mexico who used a vented stove instead of the traditional indoor open
fire, experienced improved respiratory health on par with a pack-a-day smoker kicking the
habit, according to a recent study. The study, which analyzed the first year of data in an
ongoing project examining the impact of the use of vented stoves over traditional indoor
open fires, was reported in the October 1 issue of the American Journal of Respiratory and
Critical Care Medicine, published by the American Thoracic Society. An estimated two
billion people around the world rely on biomass fuel for cooking, typically over unvented
indoor fires. These indoor fires generate high levels of pollutants such as carbon
monoxide, particulate matter and nitrogen dioxide. One recent analysis put exposure to
indoor biomass smoke among the world's top ten environmental causes of mortality and
morbidity. The "Patsari" stove was designed to address this problem, and has
been shown in previous research to reduce indoor air pollution concentrations by an
average of 70 percent. However, until now, no research has directly evaluated the health
effects on the women who use them. "We wanted to know whether the Patsari stove would
make a measurable difference in the health of people who were actually using it,"
said Horacio Riojas-Rodríguez, of the Instituto Nacional de Salud Pública, and
researcher on the study. To do so, Dr. Riojas and colleagues followed women in more than
500 households from Central Mexico, who had been randomized to receive the new Patsari
stove at the beginning of the study, or upon its conclusion. Each participant answered a
symptom questionnaire at the outset of the study and every month thereafter for ten
months. They also underwent an average of four spirometric tests during the study. Fewer
than a third of women assigned to receive the Patsari stove reported "mainly"
using it, and another 20 percent reported that they used it in conjunction with the open
fire, and fully half reported mainly using the traditional open wood fire, despite having
been assigned to the intervention group.
Rethinking Alzheimer's disease and
its treatment targets
The standard explanation for what causes Alzheimer's is known as the amyloid hypothesis,
which posits that the disease results from of an accumulation of the peptide amyloid beta,
the toxic protein fragments that deposit in the brain and become the sticky plaques that
have defined Alzheimer's for more than 100 years. Billions of dollars are spent yearly
targeting this toxic peptide — but what if this is the wrong target? What if the
disease begins much earlier, fueled by a natural process? Reporting in the current edition
of the journal Neurobiology of Aging, UCLA professor of psychiatry George Bartzokis argues
just that and says that a better working hypothesis is the "myelin
model.""The greatest promise of the myelin model of the human brain is its
application to the development of new therapeutic approaches," Bartzokis said. Like
insulation around wires, myelin is a fatty sheath that coats our nerve axons, allowing for
efficient conduction of nerve impulses. It is key to the fast processing speeds that
underlie our higher cognitive functions and encoding of memories. But the lifelong,
extensive myelination of the human brain also makes it uniquely vulnerable to damage. The
myelin model's central premise is that it is the normal, routine maintenance and repair of
myelin throughout life that ultimately initiates the mechanisms that produce degenerative
diseases like Alzheimer's. That is, the amyloid-beta peptide and the tau peptide, which is
also implicated in Alzheimer's, as well as the signature clinical signs of the disease,
such as memory loss and, ultimately, dementia, are all byproducts of the myelin breakdown
and repair processes. "The pervasive myelination of our brain is the single most
unique aspect in which the human brain differs from other species," said Bartzokis,
who is a member of the Laboratory of Neuro Imaging in the UCLA Department of Neurology and
a member of UCLA's Brain Research Institute. Myelin is produced by oligodendrocytes,
specialized glial cells that themselves become more vulnerable with age. Bartzokis notes
that myelination of the brain follows an inverted U-shaped trajectory, growing strongly
until our 50s, when it very slowly begins to unravel as we age. The myelin that is
deposited in adulthood ensheaths increasing numbers of axons with smaller axon diameters
and so spreads itself thinner and thinner, Bartzokis said. As a result, it becomes more
susceptible to the ravages of age in the form of environmental and genetic insults and
slowly begins to break down faster than it can be repaired. The exclusive targeting of the
amyloid-beta peptide for many years is understandable because the same genes and enzymes
involved in controlling myelination and myelin repair are, ironically, also involved in
the production of amyloid-beta proteins. Bartzokis' point is that the amyloid beta may
actually develop as a result of the natural process of the repair and maintenance of
myelin. "So the breakdown that leads to Alzheimer's and other age-related brain
diseases, such as Parkinson's, may begin much earlier, before the formation of the protein
deposits that are used to define these diseases," Bartzokis said.
New links among alcohol abuse,
depression, obesity in young women found
There is new evidence that depression, obesity and alcohol abuse or dependency are
interrelated conditions among young adult women but not men. Using data collected when
young adults were 24, 27 and 30 years of age, a team of University of Washington
researchers found that nearly half the sample of 776 young adults tracked during the study
met the criteria for one of these conditions at each of these time points. "The
proportion of people with all three of these conditions at any one point is small,"
said Carolyn McCarty, the lead author of a new study and a UW research associate professor
of pediatrics and psychology. "For women there is a great deal of overlap between
these common emotional and health problems that span early adulthood. Men may develop one
of these conditions but they don't tend to lead another one later on." "These
conditions are major public health problems. They take a toll on families and community
and are not subject to quick fixes. It requires a lot of time, money and energy to treat
them."
Adolescent alcohol exposure may
lead to long-term risky decision making
Picture this. A bunch of adolescent rats walk into a bar and start consuming Jell-O shots.
Lots of them. Then, three weeks later, some of those party rats are given the choice of
pushing one lever that always will give them two sugary pellets or another lever that will
give them a larger but uncertain reward of either four or zero treats. The
alcohol-consuming rats tend to opt for uncertain rewards while a control group of
teetotaling rodents match their choice well to whichever lever had the probability giving
the larger reward. That's what happened in a scenario created by University Washington
scientists investigating the neurobiological underpinnings of a link between adolescent
alcohol abuse and later adult decision-making impairments. The research, being published
this week in the online edition of the Proceedings of the National Academy of Sciences,
appears to show a causal link between early heavy drinking and adult decision-making.
"We know early exposure to alcohol and other substances is a predictor of later
substance abuse in humans. It is a novel concept to think that early exposure might have
long-term cognitive effects. But we can't test this on people. This model using rats lends
support to causal link between early alcohol use and later increased risky decision
making," said Nicholas Nasrallah, a UW psychology doctoral student and co-author of
the study. "We can't establish causal links based on existing human data but this
animal model allowed us to establish this link," said corresponding author Ilene
Bernstein, a UW professor of psychology and faculty member of the program in neurobiology
and behavior. "Scientists believe regions of the brain, including those implicated in
decision making, are slow to develop and development extends into adolescence. This study
shows that these late-developing structures in rats are affected by high alcohol
use."
People with type 2 diabetes
improved muscular strength
Physical therapist-directed exercise counseling combined with fitness center-based
exercise training can improve muscular strength and exercise capacity in people with type
2 diabetes, with outcomes similar to those of supervised exercise, according to a
randomized clinical trial published in the September issue of Physical Therapy, the
scientific journal of the American Physical Therapy Association (APTA). Type 2 diabetes is
associated with numerous health complications, including a decline in muscular strength
and exercise capacity. Studies show that a decline in muscular strength increases the risk
of loss of physical function and that a decline in exercise capacity increases the risk of
cardiovascular and all-cause mortality. "Improving muscular strength and exercise
capacity in people with type 2 diabetes is crucial to preventing loss of physical function
and decreasing comorbidity and mortality in these patients," said lead researcher J.
David Taylor, PT, PhD, CSCS, assistant professor in the Department of Physical Therapy at
the University of Central Arkansas. Supervised exercise programs improve both muscular
strength and exercise capacity in people with type 2 diabetes; however, Medicare and other
health insurance programs do not currently reimburse physical therapists and other
clinicians for these exercise programs. In this study, 24 people with type 2 diabetes were
randomly allocated to either an experimental group that received two months of physical
therapist-directed exercise counseling and fitness center-based exercise training or a
comparison group that received two months of laboratory-based, supervised exercise.
Exercise training for all participants consisted of resistance training (chest press, row,
and leg press exercises) and aerobic training (walking or jogging on a treadmill) as
recommended for people with type 2 diabetes by the American Diabetes Association and the
American College of Sports Medicine. Participants in the experimental group received a
face-to-face counseling session at baseline and one month after baseline, weekly 10-minute
telephone calls, and seven-day-per-week access to a local fitness center. Each participant
in the comparison group received the same prescribed exercise program as the experimental
group, but in a supervised environment.
Fungus enhances susceptibility of
resistant malaria mosquito to pesticides
In areas where malaria mosquitoes have become resistant to chemical pesticides,
mosquito-killing fungi can be an effective tool. Fungal spores can effectively infect and
kill malaria mosquitoes, even those that are resistant to pesticides. Moreover, the
mosquitoes become more susceptible to the pesticides as the fungal infection increases.
Researchers from Wageningen University and their colleagues from South Africa have
published an article on this effect in the prestigious journal PNAS (Proceedings of the
National Academy of Sciences) of this week. Malaria mosquitoes are becoming increasingly
resistant to pesticides. As a result, malaria is difficult to control. Besides the
existing chemical pesticides such as DDT and pyrethroids, which are applied indoors and on
mosquito nets, there are few options for mosquito control. The use of insect-killing fungi
is a novel biological control method for malaria mosquitoes that was developed in 2005 in
cooperation with Wageningen researchers. The spores of the fungi can infect mosquitoes
upon contact and kill them within several days. Moreover, a fungal infection reduces the
mosquito's appetite and slows the development of malaria parasites inside the mosquito.
Together with her colleagues in South Africa, the Wageningen researcher Marit Farenhorst
tested these fungi for the first time on various species of pesticide-resistant malaria
mosquitoes. In the laboratory in Johannesburg, the research team compared the
effectiveness of fungi on mosquitoes that are susceptible to insecticides and their
relatives who are resistant. The fungus Beauveria bassiana was able to kill both
susceptible and resistant malaria mosquitoes. This indicates that malaria mosquitoes that
are resistant to the pesticide are not resistant to the fungus.
Patient panel for skin disease
research
People who suffer from skin disease are being asked to help make research more effective
by joining a new ‘Patient Panel’. Experts in the Centre of Evidence Based
Dermatology (CEBD) at The University of Nottingham say patients and people who care for
patients could make a valuable contribution to their research into skin disease and its
treatment. Professor Hywel Williams, Director of CEBD, said: “We have a strong record
of involving patients and carers in our research. However, in the past this has been done
on an individual group or study basis. We want to bring all this together to create a more
effective research environment and to give more support to people who want to get involved
in our research.” CEBD wants to hear from people who are affected by common skin
disorders, such as eczema, psoriasis, acne and skin cancer as well as rare skin
conditions. The new panel would meet one to two times a year for training events to ensure
that those taking part in research activities are given the help and support they deserve.
Members of the panel will have the opportunity to become involved in a wide range of
research development activities and to become patient advocates of CEBD by promoting the
centre’s work in their local community. The first training event will take place at
Attenborough Nature Reserve in Nottingham on Monday November 9 2009. Professor Williams
said “The driving force of our work is the needs of our patients. This is their
chance to have a say on the direction of dermatology research, to share their experiences
in a positive way, to learn more about our work and be actively involved in improving
treatments for patients with skin disease.”
Blocking signal molecule can
prevent growth of large intestine and colon cancer
By seeing what substances and molecules affect the development of our diseases, we can
develop drugs that prevent or cure diseases. In her dissertation at Kalmar University in
Sweden, Ann Novotny has found that the signal molecule acetylcholine (ACh) is important
for the progress of cancer of the large intestine and colon, knowledge that is important
to factor in when developing drugs that block the effects of Ach on tumor cells. Cancer of
the large intestine and colon is the third most common cancer form in the Western world.
Survival over a five-year period in Sweden is roughly 56 percent, but depends on how far
the cancer has spread when it is discovered. It is known that the cancer has developed
ways to signal in order to be able grow and spread independently of the regulatory systems
of normal cells. In order to increase the number of survivors, it is important to map this
signaling so that new forms of treatment for the cancer can be devised. Ann Novotny
studied the signaling used by the cancer in a portion of large intestinal and colon
cancer. She found that there are receptors for opioids, such as morphone, on tumor cells.
If morphine is supplied to these cells the protein urokinase is released, which the cancer
cells can use to enhance their capacity to spread. She also studied the nerve signaling
molecule acetylcholine (ACh) and discovered that the cancer cells both build up and
degrade the molecule. The study shows that the molecule is constantly released from the
tumor cells and binds to a special receptor on the same cells, which leads to increased
cell production as well as increased production of urokinase, which enhances the ability
of the cancer cells to spread. These receptors can also be activated by nicotine, but also
by the peptide SLURP-1 (secreted mammalian Ly-6/urokinase plasminagen activator
receptor-related protein-1).
No Evidence to Support Ovarian
Cancer Screening
In an Australian first, leading experts and organizations have agreed a position statement
on screening for ovarian cancer, Australia's leading cause of death from gynecological
malignancy. According to a National Breast and Ovarian Cancer Centre (NBOCC) position
statement published in the October edition of the Australian and New Zealand Journal of
Obstetrics and Gynaecology (published by Wiley-Blackwell), there is no evidence to support
the use of any test, or combination of tests currently available, to screen asymptomatic
women for ovarian cancer on an individual basis or through a population-based screening
approach. The position was agreed at a NBOCC Expert Forum in Sydney, which brought
together key stakeholders in ovarian cancer across Australia. NBOCC's position statement,
Population screening and early detection of ovarian cancer in asymptomatic women, has been
endorsed by the Royal Australian and New Zealand College of Obstetricians and
Gynaecologists, the Royal Australian College of General Practitioners, the Australian
Society of Gynecologic Oncologists, Cancer Council Australia and the Screening
Subcommittee of the Australian Government Department of Health and Ageing. Each year in
Australia about 1300 women are diagnosed with ovarian cancer. However, over 70 per cent of
women are diagnosed when the disease is advanced and difficult to treat successfully. Only
four out of ten women will survive five years beyond their diagnosis.
The American Cancer Society (ACS) -
Hand-in-Hand with Drug makers
The pharmaceutical giant, AstraZeneca, is a multimillion-dollar donor to the ACS.
AstraZeneca influences every leaflet, poster, and commercial product produced by the ACS
Breast Cancer Awareness campaign. It's no wonder these publications focus almost
exclusively on mammography while ignoring carcinogenic industrial chemicals and their
relation to breast cancer. When it founded Breast Cancer Awareness Month in 1985,
AstraZeneca (formerly known as Zeneca before it merged with the Swedish pharmaceutical
company Astra) was owned by Imperial Chemical Industries, a leading international
manufacturer of industrial chemicals and carcinogenic pesticides. National Breast Cancer
Awareness Month is a masterful public relations coup for AstraZeneca, providing the
company with valuable, albeit undeserved, goodwill from millions of American women.
The American Cancer Society (ACS) -
Hand-in-Hand with Polluters
The degree of collusion between the ACS and the chemical industry became clear to Marty
Koughan, a public television producer, in 1993, when he was working on a documentary about
pesticide dangers to children for PBS's Frontline. Koughan's investigation relied heavily
on "Pesticides in the Diet of Children," an embargoed, groundbreaking report
from the National Academy of Sciences. The report declared the nation's food supply
"inadequately protected" from cancer-causing pesticides and a significant threat
to children's health.
The American Cancer Society and
toxines
The American Cancer Society (ACS) has not only remained silent about known carcinogens
from our midst, it has lent its considerable influence and media muscle to help industry
trivialize such risks. Thumbing its nose at an impressive body of legislative and
regulatory precedents such as the Delaney amendment, which until 1996 banned the addition
of known carcinogens to food products, the ACS has consistently rejected the relevance of
animal evidence as predictive of human risk. (In direct contradiction to previous ACS
protests and statements, Eyre claims the Society had not supported Delaney because it
"was just not strong or potentially effective enough.") When studies
unequivocally proved in 1971 that diethylstilbestrol (DES) caused vaginal cancers in
teenage daughters of women who had taken the drug during pregnancy, the ACS refused to
testify at congressional hearings on whether the FDA should ban the drug's use as an
animal-feed additive. (It had long ignored evidence that DES is a potent carcinogen in
rodents, known since 1939.) And in 1977, the ACS called for a congressional moratorium on
the FDA's proposed ban on saccharin, going so far as to advocate its use by nursing
mothers and babies in "moderation" despite clear-cut evidence of its
carcinogenicity in rodents and very suggestive evidence of bladder cancer in humans.
The American Cancer Society -
radiology industry ties
Just as interlocking interests with major chemical manufacturers go a long way toward
explaining the Society's resistance to prevention initiatives, close connections to the
mammography and cancer-drug industry shed light on its treatment recommendations. Five of
its past presidents were radiologists. In every move, it reflects the interests of major
manufacturers of mammogram machines and film, including Siemens, DuPont, General Electric,
Eastman Kodak, and Piker. If every premenopausal woman were to follow its mammography
guidelines, the annual revenue to health care facilities would be an additional $2.5
billion. The mammography industry conducts research for the Society and its grantees,
serves on its advisory boards, and donates considerable funds. DuPont, a major
manufacturer of mammography equipment (in addition to being a major petrochemical
manufacturer), is a primary supporter of the ACS Breast Health Awareness Program. The
company sponsors television shows and other media productions touting mammography;
produces advertising, promotional, and informational literature for hospitals, clinics,
medical organizations, and doctors; produces educational films; and lobbies Congress for
legislation promoting access to mammography services. In virtually all important actions,
the American Cancer Society (ACS) aligns itself with the mammography industry, failing to
pursue viable alternatives to mammography.
Higher Levels of Fatigue, Distress
in Resident Physicians Linked to Self-Perceived Medical Errors
Internal medicine residents who reported higher levels of fatigue and distress were more
likely to report a medical error, according to a study in the September 23/30 issue of
JAMA, a theme issue on medical education. “Medical errors and patient safety continue
to be an important concern for patients and physicians, especially since the Institute of
Medicine reported in 1999 that between 48,000 and 98,000 Americans die each year due to
preventable adverse events,” according to background information in the article.
“Fatigue and distress have been separately shown to be associated with medical
errors. The contribution of each factor when assessed simultaneously is unknown.”
Obesity Hinders Chemotherapy
Treatment in Children with Leukemia
Obesity is an important factor contributing to chemotherapy resistance and increasing
relapse rates among children with leukemia, according to recent findings published online
first in Cancer Research, a journal of the American Association for Cancer Research.
Obesity is associated with increased incidence and mortality of many types of cancer.
Leukemia is the most common cancer in children, affecting more than 2,000 children each
year in the United States alone, according to background materials in the study.
Ratchet-like Genetic Mutations Make
Evolution Irreversible
A University of Oregon research team has found that evolution can never go backwards,
because the paths to the genes once present in our ancestors are forever blocked. The
findings -- the result of the first rigorous study of reverse evolution at the molecular
level -- appear in the Sept. 24 issue of Nature. The team used computational
reconstruction of ancestral gene sequences, DNA synthesis, protein engineering and X-ray
crystallography to resurrect and manipulate the gene for a key hormone receptor as it
existed in our earliest vertebrate ancestors more than 400 million years ago. They found
that over a rapid period of time, five random mutations made subtle modifications in the
protein's structure that were utterly incompatible with the receptor's primordial form.
Switch program increases kids'
healthy eating, reduces screen time
The SwitchTM programme, 'Switch what you Do, View, and Chew', has been shown to be capable
of promoting children's fruit and vegetable consumption and lowering 'screen time'.
Researchers writing in the open access journal BMC Medicine tested the programme and
report that it offers promise for use in youth obesity prevention. Douglas Gentile, a
psychology professor from Iowa State University, USA, worked with a team of researchers to
evaluate the intervention in a group of 1,323 children and their parents from 10 schools.
He said, "Reversing the pediatric obesity epidemic has been established as a critical
priority. We tested Switch, a family-, school-, and community-based intervention aimed at
changing the key behaviors of physical activity, television viewing/screen time, and
nutrition". The Switch programme features three components, Community, School and
Family. The Community component is designed to promote awareness of the importance of
healthy lifestyles using paid advertising (such as billboards) and unpaid media (such as
letters to the editors of print publications). The School component reinforces the Switch
messages by providing teachers with materials and methods to integrate key health concepts
into the school day. Finally in the Family component, participating families receive
monthly packets containing behavioral tools to assist families in altering their health
behaviors. Gentile said, "Family components are critical for youth obesity prevention
programs because parents directly and indirectly influence children's activity and
nutrition behaviors. Parents also influence the physical and social environments that are
available to their children. The School and Community components are essential to
integrate the programme into the places where families live, work and play".
Targeted heat therapy offers new
standard treatment option for soft tissue sarcoma
Patients with soft-tissue sarcomas at high risk of spreading were 30% more likely to be
alive and cancer free almost three years after starting treatment if their tumours were
heated at the time they received chemotherapy, according to new research. The finding
bolsters the case for intensifying exploration of the strategy in other types of cancer.
The study, which found that the addition of the innovative heat technique more than
doubled the proportion of patients whose tumours responded to chemotherapy without
increasing toxicity, is also the first to show that any treatment other than surgery
followed by radiation can prolong survival of this type of patient. "These findings
provide a new standard treatment option and we believe they are likely to change the way
many specialists treat these tumours," said the study's leader, Professor Rolf
Issels, a professor of medical oncology at Klinikum Grosshadern Medical Center at the
University of Munich in Germany, who presented the results today (Tuesday 22 September) in
Berlin at Europe's largest cancer congress, ECCO 15 – ESMO 34 [1]. "But the
implications of these findings are more far-reaching," Prof Issels said. "This
is also the first clear evidence that targeted heat therapy adds to chemotherapy. We
expect our findings will encourage other researchers to test the approach in other locally
advanced cancers. Targeted heat therapy has already shown promise in recurrent breast and
locally advanced cervical cancer in combination with radiation and studies combining it
with chemotherapy in other localised tumours such as those in the pancreas and rectum are
ongoing." Soft tissue sarcomas involve cancer that starts in the soft, supporting
tissues of the body, such as muscle, fat, blood vessels, nerves, tendons, tissue around
the joints and deep layers of the skin. They are relatively rare, accounting for about
three percent of all cancers, but are more common in children and young adults. Surgery is
the primary treatment, but sometimes these tumours are difficult to remove completely, so
they are often also treated with radiotherapy and sometimes chemotherapy. However, in
cases where the disease is localised, the benefits of chemotherapy have been shown to be
limited. In high-risk patients, any relapse usually occurs within two or three years.
Survival varies widely depending on the location and severity of the tumour, with
abdominal sarcomas being the most deadly. The phase III study involved 341 patients being
treated at several centres in Europe and the United States between July 1997 and November
2006 for locally advanced soft tissue sarcomas that were at high risk of recurrence and
spread. More than half of the tumours were located in the abdomen, while the rest were in
the arms and legs. All patients were given chemotherapy before and after surgery and
radiotherapy.
Prostate cancer patients on hormone
therapy at increased risk for various heart diseases
New research has found that hormone therapy used to treat men with advanced prostate
cancer is associated with an increased chance of developing various heart problems. Some
choices of therapy appear, however, to be less risky than others. Researchers told
Europe's biggest cancer congress, ECCO 15 – ESMO 34 [1], in Berlin today (Tuesday 22
September) that the findings of their study, the largest and most comprehensive to date on
the issue, indicate that doctors need to start considering heart-related side effects when
they prescribe endocrine therapy for prostate cancer and might want to refer patients to a
cardiologist before starting treatment. A few smaller studies have indicated that some
types of hormone therapy increase the risk of coronary heart disease and heart attacks in
prostate cancer patients, but others have found no increased risk. This is the first large
study to investigate how he broader range of hormone therapies affect a wider range of
heart problems and provides for the first time a detailed picture of the impact of each
sort of hormone therapy on individual types of heart trouble. "If we have observed a
causative effect, then for all hormone therapies put together, we estimate that compared
with what's normal in the general population, about 10 extra ischaemic heart disease
events a year will appear for every 1,000 prostate cancer patients treated with such
drugs," said the study's leader, Ms Mieke Van Hemelrijck, a cancer epidemiologist at
King's College in London. "However, not all types of therapy were associated with the
risk of heart problems to the same degree. We found that drugs which block testosterone
from binding to the prostate cells were associated with the least heart risk, while those
that reduce the production of testosterone were associated with a higher risk. This may
have implications for treatment choice." Prostate cancer is diagnosed in more than
670,000 men each year worldwide, making it the second most common cancer among men
worldwide, after lung cancer. Hormone therapy is a mainstay of treatment when the cancer
is locally advanced and when it has spread to more distant parts of the body, but is
increasingly being used in earlier stages of the disease. It involves either removing the
testicles to eliminate the main source of testosterone production, injections of
gonadotropin releasing hormone agonists to dramatically reduce the production of
testosterone from the testicles or anti-androgen pills, which do not reduce the amount of
testosterone produced but block it from attaching the prostate cells. Doctors sometimes
use a combination of those approaches. In the study, researchers analysed the link in
30,642 Swedish men with locally advanced or metastatic prostate cancer who had received
hormone therapy as primary treatment for their disease between 1997 and 2006. The men were
followed for an average of three years. The researchers calculated the risk of developing
ischaemic heart disease, heart attacks, arrhythmia and heart failure requiring
hospitalisation as well as the risk of dying from these heart diseases by comparing the
rates among the cancer patients with what's normal in the general Swedish population. Most
patients got one of the three hormone treatment choices, but 38% got a combination of the
two types of drugs.
Pancreatic fat levels may help
predict diabetes, UT Southwestern researchers say
Researchers have long suspected that overweight people tend to have large fat deposits in
their pancreases, but they've been unable to confirm or calculate how much fat resides
there because of the organ's location.Until now. Scientists at UT Southwestern Medical
Center are the first in the U.S. to use an imaging technique called magnetic resonance
spectroscopy (MRS) to measure the amount of pancreatic fat in humans. Though scientists
worldwide already use MRS to investigate a number of diseases including breast cancer and
epilepsy, the UT Southwestern group has successfully used the noninvasive method to
measure pancreatic fat. Findings from a new UT Southwestern study available online and in
a future issue of the Journal of Clinical Endocrinology and Metabolismsuggest that
measuring pancreatic fat content in people could one day serve as an effective clinical
tool to identify those at high risk of diabetes and monitor interventions designed to
prevent the disease. "These are very early results, but if they hold true, pancreatic
MRS would be a fast and noninvasive test to screen people at risk for diabetes either
because they're obese or they have a family history of type 2 diabetes, or metabolic
syndrome," said Dr. Ildiko Lingvay, assistant professor of internal medicine at UT
Southwestern and lead author of the study. "It could potentially tell physicians
which patients are most likely to develop diabetes in the near future and thus are in need
of more aggressive interventions." MRS is a specialized technique similar to magnetic
resonance imaging (MRI). It uses no radiation and is completely noninvasive. The test
generally takes 20 to 30 minutes. Whereas an MRI can tell clinicians where a tumor is
located, MRS can tell those physicians whether the tumor is malignant by providing
biochemical information about specific tissues in the body rather than simply detecting
the existence of those tissues, Dr. Lingvay said.
New device could more effectively
alleviate menstrual cramp pain
While most women experience minor pain during menstruation, for others, the pain can be
severe enough to interfere with everyday activities and require medication. New research
to be presented at the 2009 American Association of Pharmaceutical Scientists (AAPS)
Annual Meeting and Exposition will reveal initial findings of safety surrounding a new
device that may more effectively treat menstrual pain. "The goal of our study was to
find a better way to treat menstrual cramps," said Giovanni M. Pauletti, Ph.D.,
associate professor at the University of Cincinnati and the study's presenter as well as
past chair of AAPS' National Biotechnology Conference Planning Committee. "Existing
oral medications cause significant gastrointestinal side effects for women, creating
additional discomfort while alleviating menstrual pain. Results from our Phase I clinical
trials show that this new vaginal device safely delivers at least 10-times more drug to
the uterus as a tablet of equivalent dose." The study, which was sponsored by UMD,
Inc., a Cincinnati drug delivery company, and conducted at Women's Health Research, Inc.
involved 18 study participants, aged 18-45 years with menstrual cycles between 25-30 days.
During the mid-follicular phase of the first menstrual cycle (days 7-11), nine study
participants received an oral dose of 10 mg of ketorolac (Toradol®), a non-steroidal
anti-inflammatory medication; while nine women received a tampon coated with 10 mg of
ketorolac. During the second menstrual cycle, each subject received the opposite
treatment. The results of the study demonstrated that the medication administered
vaginally does not cause significant side effects but accumulates more efficiently in the
desired uterine tissue than using the oral medication.
Experimental approach may reverse
rheumatoid arthritis and osteoporosis
Researchers have identified a mechanism that may keep a well known signaling molecule from
eroding bone and inflaming joints, according to an early study published online today in
the Journal of Clinical Investigation. Bone is continually recycled to maintain its
strength through the competing action of osteoclasts, cells that break down aging bone,
and osteoblasts, which build new bone. Osteoclasts also play a central role in common
diseases that erode bone, where two signaling molecules, TNF? and RANKL, cause too much
bone breakdown. Both are known to turn on the nuclear factor kappa B complex (NF-?B),
which turns on genes that cause the stem cell precursors of osteoclasts to mature and
start eating bone. While both TNF? and RANKL encourage bone loss, the current study argues
that TNF? and RANKL have different effects on levels of a key inhibitory protein within
the NF-?B pathway called NF-?B p100, with important consequences for drug design. The
NF-?B pathway as a whole signals for more active osteoclasts, but NF-?B p100 (p100)
interferes with the ability of that same pathway to pass on the bone loss signal. While
both TNF? and RANKL activate NF-?B signaling, RANKL efficiently converts p100 into a form
that no longer blocks NF-?B pathway signaling and that leads to bone loss. In contrast,
the current study is the first to show that TNF? lets p100 build up. Thus, TNF? both
causes bone loss through NF-?B signaling and limits it via p100 accumulation. Experiments
found further that mice genetically engineered to lack NF-?B2p100 suffered more severe
joint erosion and inflammation than their normal littermates in the face of TNF?. TNF?,
but not RANKL, also increased levels of a protein in osteoclast precursors called TNF
receptor-associated factor 3 (TRAF 3), which may help NF-?B p100 block osteoclast
formation and inflammation. "While further studies will be required to confirm and
detail this mechanism, our results argue strongly that increasing levels of either TRAF3
or NF-?B p100 could represent a powerful new way to limit bone destruction and
inflammation-induced bone loss seen in osteoporosis and rheumatoid arthritis," said
Brendan Boyce, M.D., professor within the Department of Pathology and Laboratory Medicine
at the University of Rochester Medical Center, and the study's corresponding author.
"NF-?B p100 levels may vary with each person's genes, making some more susceptible to
TNF?-driven disease. Future solutions may be local delivery of p100 into diseased joints
via gene therapy, or to target with a drug the enzyme, NIK, which otherwise limits the
p100 supply."
New device finds early signs of eye
disease in preemies
Tell-tale signs of a condition that can blind premature babies are being seen for the
first time using a new handheld device in a study at Duke University Medical Center. The
technology, developed in part by Duke biomedical engineers, uses spectral domain optical
coherence tomography (SD OCT) to create a 3-D picture of the back of the eye. "This
new tool is changing the way we identify eye conditions in infants," says Cynthia
Toth, MD, an ophthalmologist at the Duke Eye Center, who is leading the study that appears
online this month in the journal Ophthalmology. Retinopathy of prematurity (ROP) is one of
the most common causes of vision loss in children, affecting about 16,000 babies each
year, according to the National Eye Institute. It occurs when babies are born prematurely
and their retinal blood vessels don't develop fully. Instead, the vessels grow abnormally
and are prone to leaking and contracting. That can pull the retina out of position,
causing retinal detachments that can lead to visual loss and blindness. Current screening
for ROP is based on two-dimensional images taken either with an ophthalmoscope or a camera
placed directly on the infant's cornea. "Examining the retina with these methods is
like looking at the surface of the ocean and only seeing dimly into the shallow
water," says Toth, a professor of ophthalmology and biomedical engineering. "You
cannot see what lies below." SD OCT, on the other hand, uses a narrow beam of light
to create a 3-D high-resolution map of the intricate detail in the retina's layers.
"This is like looking into an aquarium from the side, where all the fish at every
depth are visible," Toth says. Ophthalmologists at Duke Eye Center pioneered and have
been using OCT to accurately diagnose adult eyes for more than a decade, and in the past
two years, Toth has been studying the application of this technology for retinal diseases
in children.
DARPA-Funded Duke Study to Detect
Viral Infection Before Symptoms Appear
The Defense Advanced Research Projects Agency (DARPA), the research arm of the U.S.
Department of Defense, has awarded Duke University $19.5 million for an effort led by the
Duke Institute for Genome Sciences & Policy (IGSP) to design a portable, easy-to-use
diagnostic device that can reveal who is infected with an upper respiratory virus before
the first cough or sneeze.
Can an over-the-counter
vitamin-like substance slow the progression of Parkinson's disease?
Rush University Medical Center is participating in a large-scale, multi-center clinical
trial in the U.S. and Canada to determine whether a vitamin-like substance, in high doses,
can slow the progression of Parkinson's disease, a neurodegenerative disorder that affects
about one million people in the United States. "At present, the very best therapies
we have for Parkinson's can only mask the symptoms – they do not alter the underlying
disease," said neurologist Dr. Katie Kompoliti, a specialist in movement disorders.
"Finding a treatment that can slow the degenerative course of Parkinsons's is the
holy grail of Parkinson's research." The substance being tested, called coenzyme Q10,
is produced naturally in the body and is an important link in the chain of chemical
reactions that produce energy in mitochondria, the "powerhouses" of cells. The
enzyme is also a potent antioxidant – a chemical that "mops up" potentially
harmful chemicals generated during normal metabolism. Several studies have shown that
Parkinson's patients have impaired mitochondrial function and low levels of coenzyme Q10.
Moreover, laboratory research has demonstrated that coenzyme Q10 can protect the area of
the brain damaged in Parkinson's. The Phase III clinical trial, a large, randomized study
with a control group, follows an earlier investigation that tested several doses of
coenzyme Q10 in a small group of patients with early-stage Parkinson's disease. The
highest dose, 1,200 mg, appeared promising. Over the course of 16 months, patients taking
this dose experienced significantly less decline than other patients in motor (movement)
function and ability to carry out activities of daily living, such as feeding or dressing
themselves. But researchers involved in the study, including Kompoliti, were cautious
about their findings, citing the need for a more extensive review to confirm the results.
Breathing technique can reduce
frequency, severity of asthma attacks
As the health care reform debate turns to cutting costs and improving treatment outcomes,
two professors at Southern Methodist University in Dallas are expanding a study that shows
promise for reducing both the expense and suffering associated with chronic asthma. Thomas
Ritz and Alicia Meuret, both in SMU's Psychology Department, have developed a four-week
program to teach asthmatics how to better control their condition by changing the way they
breathe. With the help of a four-year, $1.4 million grant from the National Institutes of
Health, they plan to engage 120 Dallas County patients in four weeks of breathing training
by the study's projected end in July 2011. Their co-investigators include David
Rosenfield, also of SMU's Psychology Department, and Mark Millard, M.D., of Baylor
University Medical Center in Dallas. More than 22 million Americans suffer from asthma at
an estimated annual economic cost of more than $19 billion, according to the American Lung
Association. The number of cases doubled between 1980 and 1995, prompting the U.S.
Department of Health and Human Services to classify the disease as an epidemic in 2000.
During an attack, sufferers tend to hyperventilate, breathing fast and deep against
constricted airways to fight an overwhelming feeling of oxygen deprivation. Unfortunately,
this makes the problem worse by lowering the body's carbon dioxide levels, which restricts
blood flow to the brain and can further irritate already hypersensitive bronchial
passages. Patients who "overbreathe" on a sustained basis risk chronic CO2
deficiencies that make them even more vulnerable to future attacks. Rescue medications
that relieve asthma symptoms do nothing to correct breathing difficulties associated with
hyperventilation.
You can't trust a tortured brain -
Neuroscience discredits coercive interrogation
According to a new review of neuroscientific research, coercive interrogation techniques
used during the Bush administration to extract information from terrorist suspects are
likely to have been unsuccessful and may have had many unintended negative effects on the
suspect's memory and brain functions. A new article, published by Cell Press on September
21st in the journal, Trends in Cognitive Science, reviews scientific evidence
demonstrating that repeated and extreme stress and anxiety have a detrimental influence on
brain functions related to memory. Memos released by the US Department of Justice in April
of 2009 detailing coercive interrogation techniques suggest that prolonged periods of
shock, stress, anxiety, disorientation and lack of control are more effective than
standard interrogatory techniques in making subjects reveal truthful information from
memory. "This is based on the assumption that subjects will be motivated to reveal
veridical information to end interrogation, and that extreme stress, shock and anxiety do
not impact memory" says review author, Professor Shane O'Mara from the Institute of
Neuroscience at Trinity College in Dublin, Ireland. "However, this model of the
impact of extreme stress on memory and the brain is utterly unsupported by scientific
evidence." Psychological studies suggest that during extreme stress and anxiety, the
captive will be conditioned to associate speaking with periods of safety. For the captor,
when the captive speaks, the objective of gaining information will have been obtained and
there will be relief from the unsavory task of administering these conditions of stress.
Therefore, it is difficult or impossible to determine during the interrogation whether the
captive is revealing truthful information or just talking to escape the torture. Research
has also shown that extreme stress has a deleterious effect on the frontal lobe and is
associated with the production of false memories. Neurochemical studies have revealed that
the hippocampus and prefrontal cortex, brain regions integral to the process of memory,
are rich in receptors for hormones that are activated by stress and sleep deprivation and
which have been shown to have deleterious effects on memory. "To briefly summarize a
vast, complex literature, prolonged and extreme stress inhibits the biological processes
believed to support memory in the brain," says O'Mara. "For example, studies of
extreme stress with Special Forces Soldiers have found that recall of previously-learned
information was impaired after stress occurred." Waterboarding in particular is an
extreme stressor and has the potential to elicit widespread stress-induced changes in the
brain.
UCF professor finds new way deadly
food-borne bacteria spread
University of Central Florida Microbiology Professor Keith Ireton has uncovered a
previously unknown mechanism that plays an important role in the spread of a deadly
food-borne bacterium. Listeria monocytogenes is a bacterium that can cause pregnant women
to lose their fetuses and trigger fatal cases of meningitis in the elderly or people with
compromised immune systems. The bacterium has been linked to outbreaks traced to food
processing plants in the U.S. and Canada. In 2002, a multi-state outbreak of listeriosis
– the serious disease caused by Listeria -- resulted in 46 confirmed cases, seven
deaths and three stillbirths or miscarriages. Those cases in eight states were linked to
people eating contaminated sliced turkey deli meat. From January to August 1985, there was
another outbreak with 142 cases of listeriosis. Scientists have long known that Listeria
spreads from one human cell to another. Bacteria growing in one cell move fast enough to
create a finger-like structure that protrudes from the cell and pushes into an adjacent
cell. The bacteria then infect the adjacent cell. Ireton and his team have discovered a
previously unknown second process that aids in the spread of bacteria to healthy cells.
The process, which gradually overwhelms the second cell's ability to defend itself from
infection, is featured in this week's edition of the science journal Nature Cell Biology.
The plasma membrane, or outer layer, of healthy human cells normally exhibits tension.
Such tension might be expected to prevent Listeria from spreading to adjacent uninfected
cells. However, Ireton's lab found that a Listeria protein called InlC appears to relieve
tension at the plasma membrane in infected cells, making it easier for moving bacteria to
deform the membrane and then spread into adjacent, healthy cells.
New genetic link between cardiac
arrhythmias and thyroid dysfunction identified
Genes previously known to be essential to the coordinated, rhythmic electrical activity of
cardiac muscle -- a healthy heartbeat -- have now also been found to play a key role in
thyroid hormone (TH) biosynthesis, according to Weill Cornell Medical College researchers.
The authors' findings, published online this week by the peer-reviewed journal Nature
Medicine, suggest that mutations of either of two gene products -- proteins called KCNE2
and KCNQ1 -- already known to be involved in human cardiac arrhythmias, could also cause
thyroid dysfunction. "It has long been known that the thyroid influences cardiac
function and cardiac arrhythmias," says study senior author Dr. Geoffrey W. Abbott,
associate professor of pharmacology in medicine at Weill Cornell Medical College,
"but our findings demonstrate a novel genetic link between inherited cardiac
arrhythmia and thyroid dysfunction." Additionally, it is the authors' suggestion that
assessment of the thyroid status of patients with KCNE2- and KCNQ1-linked cardiac
arrhythmias could in some cases reveal a potential endocrine component to their cardiac
arrhythmias that may not have been previously determined. This, in turn, could indicate
treatment of the thyroid condition, with potentially beneficial effects on cardiac
function. KCNQ1 and KCNE2 were each recognized more than a decade ago as forming potassium
channels in cardiac muscle that help end each heartbeat in a timely fashion. Inherited
mutations in KCNQ1 and KCNE2 cause ventricular and atrial cardiac arrhythmias, previously
presumed to be due entirely to the role of these proteins in cardiac muscle. The
researchers have now discovered that KCNQ1 and KCNE2 also form a potassium channel in the
thyroid gland. "When the thyroid does not produce enough TH, a person may experience
symptoms such as fatigue and a lowered heart rate, but there is also a more complex
interplay between thyroid function, cardiac structure and cardiac arrhythmias. Our new
findings may begin to explain some of these interrelationships," explains Dr. Abbott.
While studying mice that had the KCNE2 gene removed from their genome, the researchers
observed that the animals developed symptoms of hypothyroidism, especially during
pregnancy, and gave birth to pups with dwarfism, alopecia (baldness) and cardiomegaly
(enlarged heart).
Scientists discover key factor in
regulating placenta and fetal growth
Scientists funded by the Biotechnology and Biological Sciences Research Council (BBSRC)
have shown that a common biological protein molecule called SHP-2 is crucial for
encouraging placenta growth. The research is published today in Endocrinology. Dr Melissa
Westwood, one of the team at the University of Manchester said: "For fetuses to grow
well in the womb they need to get nutrients and oxygen from their mother. These come via
the placenta and so as the fetus grows and its demand on mum increases, the placenta also
must increase in size. If the placenta doesn't grow properly, the fetus is unable to
receive all it needs from the mother and its growth is restricted. This can impact
seriously on the health of the newborn. Furthermore we have learned recently that it
dramatically increases the risk of ill health in adult life." The researchers have
investigated a group of proteins called the insulin-like growth factors (IGF). They have
discovered that SHP-2, a molecule within placental cells, is a crucial mediator of the
effects of IGFs in stimulating the placenta to grow. Dr Westwood continued: "We know
that placentas need an array of factors to support their growth, but until now we didn't
realise that SHP-2 was so important for ensuring that these factors do their job.
"Research from our lab and others around the world suggests that the placentas of
growth-restricted babies might not grow because they are resistant to the effects of
growth factors. We know that in many tissues in the body, SHP-2 is involved with the
action of other growth factors – not just IGF. Targeting the mediators of growth
factor actions rather than the growth factors themselves may be a good way to intervene in
cases of growth restriction – a bit like sending a positive email to all your friends
at the same time.
New blood tests promise simple,
cost-effective diagnosis of gastrointestinal cancers
Promising results from two new blood tests that can aid in the early identification of
patients with gastrointestinal (GI) cancers will be presented at Europe's largest cancer
congress, ECCO 15 – ESMO 34 [1], in Berlin today (Monday September 21). The tests
will make GI cancer detection simpler, cost-effective, and more acceptable to patients
than current methods, the researchers say. In the first study, Dr Joost Louwagie, from the
company OncoMethylome Sciences, headquartered in Liège, Belgium, will present data on the
way in which tumour markers for colorectal cancer were selected, the analytical
performance of the test and the first results from a multi-centre feasibility study.
"This test has potential to provide a better balance of performance,
cost-effectiveness and patient compliance than other options currently available for
colorectal cancer screening," he says. The scientists collected blood before surgery
from 193 patients known to have colorectal cancer, as well as from 688 controls undergoing
colonoscopy for cancer screening. DNA was extracted from the blood plasma and tested for
the presence of DNA methylation of specific genes. DNA methylation is involved in the
regulation of protein expression, and methylation or silencing of key genes has been
linked to the initiation and progression of tumours. Based on studies conducted in
colorectal tissues, methylated genes that were capable of discriminating accurately
between cancerous and normal tissues were chosen. The scientists then evaluated the
best-performing methylated genes in blood samples, with the ultimate goal of providing a
sensitive, specific and patient-friendly option for colorectal cancer screening. "We
optimised the methods of DNA extraction and methylation detection so that we could detect
low levels of methylated genes in people with colorectal cancer," says Dr Louwagie,
"and we were able to find a high frequency of two newly reported methylation genes,
SYNE1 and FOXE1, in colorectal cancer patients. The same methylation genes occurred
infrequently in non-cancerous individuals." When testing a first set of 444 controls
and 124 colorectal cancer patients, with plasma volumes ranging between 0.8 and 4.3 ml,
the sensitivity and specificity for the combination of SYNE1 and FOXE1 was 58% and 90%
respectively. Testing this marker combination in a second, independent group of 242
controls and 69 cases, the sensitivity (proportion of positives correctly identified) and
specificity (proportion of negatives correctly identified) were 56% and 91% respectively
(77% and 91% in the samples with at least 3.3 ml of plasma). The sensitivity for stage I
and II disease was 41% and 80% respectively. Colorectal cancer occurs in approximately one
in every 17 people during their lifetime and is the second leading cause of cancer death
in the United States and Europe; in these places a combined total of about 560,000 people
develop the disease each year, and 250,000 die from it. Deaths can be reduced if the
cancer is diagnosed at an early stage, when it is most treatable. Although there are
already two effective screening methods, they both have drawbacks.
How Scientists Think - Fostering
Creativity in Problem Solving
Profound discoveries and insights on the frontiers of science do not burst out of thin air
but often arise from incremental processes of weaving together analogies, images, and
simulations in a constrained fashion. In cutting-edge science, problems are often
ill-defined and experimental data are limited. To develop an understanding of the system
under investigation, scientists build real-world models and make predictions with them.
The models are tentative at first, but over time they are revised and refined, and can
lead the community to novel problem solutions. Models, thus, play a big role in the
creative thinking processes of scientists. Dr. Nancy J. Nersessian has studied the
cognitive processes that underlie scientific creativity by observing scientists at work in
their laboratories. She says, "Solving problems at the frontiers of science involves
complex cognitive processes. In reasoning with models, part of the process occurs in the
mind and part in the real-world manipulation of the model. The problem is not solved by
the scientist alone, but by the scientist - model combination. This is a highly creative
cognitive process." Her research is published in an upcoming issue of Topics in
Cognitive Science.
Immune capacity of thymus gland in
the elderly is proven
Doctor Manuel Leal is managing the Experimental Immune Virology Laboratory (in Virgen del
Rocío University Hospital and Instituto de Biomedicina de Sevilla (IBIS), where clinic
and basic science researchers work) where he leads a project to establish the functional
nature of the thymus gland in adults. So far, it has been proven that this gland keeps on
producing lymphocytes in the old age (Ferrando-Martínez et al. AGE, in press), which is a
novelty because until very recently it was considered that this organ lost its immune
capacity after the puberty. At the same time, the researchers, in collaboration with the
Dr. Antonio Ordoñez from the Hospital Cardiovascular Surgery Service, have developed a
successful method to obtain thymus samples in vivo from patients subjected to heart
surgery. These are the results of a project of excellence of the Andalusian Ministry of
Innovation, funded with 197,299 euros. The thymus is a gland with an important role in the
sexual development and maturing of the lymphatic system, which starts its function in the
foetus. After the puberty, this organ appears to gradually reduce its size and up to now,
it was believed that it stopped working. Moreover, there is a process called
immunosenescence that is the ageing of our immune system, which undergoes a loss of its
capacity of response to diseases and vaccines. This phenomenon is linked to a higher
number of infections in people and it is believed that it can affect the development of
cancer or autoimmune diseases. An important aspect of the research led by Manuel Leal is
that the thymic function in adults is very heterogeneous and is related to the ageing of
the immune system. ‘With this discovery, we have proven the importance of residual
thymopoiesis (the function of the thymus gland to produce T-lymphocytes) in aged adults by
means of a direct quantification of the thymic function', Leal said. We have specifically
worked with 65 people with an average of 68.5 years of age, who have taken a sample of
thymic tissue that was analysed later. As the thymus gland is placed just behind the
breastbone and it is very difficult to get to it, rests of in vivo thymus gland have been
used for this research for the first time ever. Until now, only ex vivo glands had been
used, after the death of patients or in lab animals.
Ozone layer depletion levelling off
A team of scientists around Ashley Jones and Jo Urban from Sweden’s Chalmers
University of Technology combined the limb measurements of US instruments SBUV, SAGE I+II
and HALOE with data from OSIRIS, SMR and SCIAMACHY on the European satellites Odin and
Envisat to analyse the long-term evolution of stratospheric ozone from 1979 to the
present. These data show a decrease in ozone from 1979 until 1997, and a small increase
since then. "Our analysis shows that upper stratospheric ozone declines at northern
and southern mid-latitudes at roughly 7% per decade during 1979–97, consistent with
earlier studies based on data from satellites and ground networks. A clear statistically
significant change of trend can be seen around 1997. The small increase (of 0.8–1.4%
per decade) observed thereafter, from 1997 to 2008, is however not yet statistically
different from a zero trend. We hope to see a significant recovery of (upper
stratospheric) ozone in the next years using longer, extended satellite time-series,"
Urban said. The thinning of the ozone layer is caused by chemicals such as human-produced
bromine and chlorine gases that have long lifetimes in the atmosphere. The Montreal
Protocol (1987) was introduced to regulate and phase out the production of these
substances. Its effect can clearly be seen in the satellite observations of ozone and
these chemicals.
Nevada professor discovers new way
to calculate body's 'Maximum Weight Limit'
Nevada professor discovers new way to calculate body's "Maximum Weight Limit"
RENO, Nev. – Most of us are familiar with the term, Body Mass Index, or BMI, as an
index to determine healthy body weight. But, calculating BMI involves a complex formula:
weight in pounds is multiplied by 703, and then divided by height in inches squared.
Charts or online calculators are then used to show a "healthy weight range"
given an individual's height that corresponds to the "healthy range BMI." For
example, a BMI chart indicates that a healthy range BMI of 19 to 24 translates to a
"healthy weight range" of 120 to 150 pounds for a 5-foot, 6-inch individual. If
this sounds way too complicated to you, you're not alone. George Fernandez, a professor of
applied statistics and director of the Center for Research Design and Analysis at the
University of Nevada, Reno, set out to give people a simpler way of calculating their
healthy weight, and one that wouldn't require charts or online calculators. In addition,
he doesn't think the "range" approach sticks in individuals' minds. "We
need a "Maximum Weight Limit, or MWL," he said, "one number that we know we
can't go over, just like a speed limit." So, using SAS software and statistical
procedures, he discovered a much simpler way of calculating a Maximum Weight Limit, which
closely corresponds to weight recommendations listed on BMI charts. But, you don't need to
calculate or know your BMI, nor do you need a chart or online calculator to figure out
your Maximum Weight Limit. Fernandez will present his Maximum Weight Limit calculation at
the Nevada Public Health Association Conference, 1:30 p.m., Sept. 22 at the University of
Nevada, Reno's Joe Crowley Student Union, Room 423. "It's a very simple calculation
that most of us can do in our heads," he explained. For men and women, there is a
baseline height and weight. For men, the baseline is 5-feet, 9-inches tall and a Maximum
Weight Limit of 175 pounds, meaning that a 5-foot, 9-inch tall man should weigh no more
than 175 pounds. For women, the baseline is 5-feet tall and a Maximum Weight Limit of 125
pounds. "These are nice round numbers that people can easily remember: 5-feet,
9-inches tall, 175 pounds for man; and 5-feet tall, 125 pounds for a woman,"
explained Fernandez.
Young age at first drink may affect
genes and risk for alcoholism
The age at which a person takes a first drink may influence genes linked to alcoholism,
making the youngest drinkers the most susceptible to severe problems. A team of
researchers, led by scientists at Washington University School of Medicine in St. Louis,
studied 6,257 adult twins from Australia. They wanted to learn whether twins who start
drinking at an early age are more likely to develop a more heritable form of alcohol
dependence than those who begin drinking later in life. The researchers found that the
younger an individual was at first drink, the greater the risk for alcohol dependence and
the more prominent the role played by genetic factors. "There seemed to be a greater
genetic influence in those who took their first full drink at a younger age," says
first author Arpana Agrawal, Ph.D. "That's very consistent with what has been
predicted in the literature and in the classification of types of alcohol dependence, but
we present a unique test of the hypothesis." Agrawal and her colleagues examined
previously collected data from identical and fraternal, male and female twins, using
statistical methods to measure the extent to which age at first drink changed the role of
heritable influences on symptoms of alcohol dependence. Using the twin model, they were
able to tease out genetic influences, shared environmental influences and non-shared
environmental factors. Agrawal's team found that when twins started drinking early,
genetic factors contributed greatly to risk for alcohol dependence, at rates as high as 90
percent in the youngest drinkers. For those who started drinking at older ages, genes
explained much less, and environmental factors that make twins different from each other,
such as unique life events, gained prominence.
New vitamin K analysis supports the
triage theory
An important analysis conducted by Children's Hospital Oakland Research Institute
scientists suggests the importance of ensuring optimal dietary intakes of vitamin K to
prevent age-related conditions such as bone fragility, arterial and kidney calcification,
cardiovascular disease, and possibly cancer (1). Vitamin K is concentrated in dark green
plants such as spinach or Swiss chard, and is either not present or present in only small
amounts in most multivitamin pills. This finding comes from Associate Staff Scientist,
Joyce McCann, PhD, and Senior Scientist, Bruce Ames, PhD, who analyzed data from hundreds
of published articles dating back to the 1970's. Their review was designed to test Dr.
Ames' "triage" theory that provides a new basis for determining the optimum
intake of individual vitamins and minerals (also called micronutrients), and has major
implications for preventive medicine. The analysis, which strongly supports his theory,
will be published in the October 2009 issue of the American Journal of Clinical Nutrition.
Dr. Ames proposed the triage theory in 2006 (2,3) to explain numerous observations from
his own lab and the scientific literature. The theory explains why diseases associated
with aging like cancer, heart disease, and dementia (and the pace of aging itself) may be
unintended consequences of mechanisms developed during evolution to protect against
episodic vitamin/mineral shortages. If correct, the triage theory has widespread
implications for public health because modest vitamin/mineral deficiencies are quite
common. The theory also suggests a new scientifically based and consistent strategy for
establishing optimal vitamin/mineral intake standards, and it provides a research strategy
to uncover early biomarkers of chronic disease. Vitamin K is known as the
"Koagulation" vitamin because about half of the 16 known proteins that depend on
vitK are necessary for blood coagulation. The other vitK-dependent proteins are involved
in a variety of different functions involving the skeletal, arterial, and immune systems.
Scientists pinpoint protein link to
fat storage
A protein found present in all cells in the body could help scientists better understand
how we store fat. Researchers at the University of Edinburgh have found that the protein
invadolysin, which is essential for healthy cell division, is present in lipid droplets
– the parts of cells used to store fat. The study also found that lower levels of
invadolysin were linked to reduced amounts of fat deposits. The findings, published in the
Journal of Cell Science, could ultimately help scientists to better understand
obesity-related complications, which can include diabetes, blood clotting and heart
disease.
Mechanism related to the onset of
various genetic diseases revealed
UAB researchers discover that the separation of 2 or more proteins due to genetic
mutations causes them to malfunction. Researchers at the Department of Biochemistry and
Molecular Biology of Universitat Autònoma de Barcelona (UAB) have revealed the process by
which proteins with a tendency to cause conformational diseases such as amyotrophic
lateral sclerosis, familial amyloidotic polyneuropathy, familial amyloidotic
cardiomyopathy, etc. finally end up causing them. Researchers have carried out an analysis
of their 3D structure and studied why these proteins finally become toxic although they
are correctly folded, an indicator that they are functioning correctly. The answer can be
found in the separation of the proteins, which under normal conditions are found in groups
of two or more, caused by a genetic mutation in their composition. Researchers believe
this discovery, published recently in the journal PLoS Computational Biology, could also
be the cause of other diseases of unknown origins. Every day cells produce thousands of
new proteins which renew themselves every second and which, by obeying the orders
prescribed in our genetic code, work towards the proper functioning of our body. However,
these proteins occasionally suffer genetic mutations which can cause changes in their
composition, thus preventing them from carrying out their functions and the activities
they are assigned. In many cases this gives way to the formation of toxic macromolecular
aggregates - amyloid fibrils - which block our body's protein quality control system and
finally provoke cell death. Protein aggregation and the misfolding of proteins can be
linked to the origin of many conformational diseases which can be either genetic or
spontaneous. The proteins involved can either have an unstructured or lineal unfolded form
such as in Alzheimer's and Parkinson's disease or Type II Diabetes, or can be globular,
showing a folded 3D-structure. The former have been widely characterised by scientists and
the process by which they unfold is known. The process leaves regions uncovered which are
in the risk of becoming aggregated and these eventually form toxic assemblies. Globular
proteins are known to be linked to hepatic, cardiac, renal and neurological disorders.
However scientists do not know exactly how they manage to aggregate despite the fact that
they are correctly folded within the body.
Regulatory role of key molecule
discovered
Discovery by Hebrew University of Jerusalem researchers of an additional role for a key
molecule in our bodies provides a further step in world-wide efforts to develop genetic
regulation aimed at controlling many diseases, including AIDS and various types of
cancers. The molecule, known as Lysyl-tRNA synthetase (or LysRS in brief) is one of the
most ancient molecules in the cell, where it has long been recognized for its contribution
in the translation of the information contained in RNA into the amino acids that make up
proteins. Amino acids are organic compounds which are present in and vital to every living
cell. Now, the Hebrew University scientists have discovered that LysRS plays an important
additional role as a central regulator controlling expression of various genes. In this
additional role, LysRS ceases its previous function at a certain point and participates in
a chain of events that causes the freeing of inhibitors that prevent expression of certain
genes. The researchers say that this research has particularly great importance, since
LysRS is known to be involved in diseases such as AIDS and cancers. The virus HIV uses the
host's cellular LysRS in the process of replication. High levels of LysRS also have been
observed in certain cancers, such as breast cancer. The specific molecular mechanisms in
these contexts remain to be discovered. An ability to understand the regulatory effect
played by LysRS in various diseases could make an important contribution to the worldwide
search for therapies that would control the "turning on" or "turning
off" of specific genes that are operative in those diseases, they emphasize.
Relieving pain affecting millions
An unprecedented gathering of some of Australia's leading authorities in pain medicine,
together with consumer groups representing chronic pain sufferers, will meet in Melbourne
today to work towards a national, coordinated approach to managing chronic pain. The
meeting has been called in recognition of the fact that one in five Australians will
suffer chronic pain in their lifetime and up to 80% of people currently living with
chronic pain are missing out on treatment that could improve their health and quality of
life. The MBF Foundation's landmark report, The High Price of Pain, originally highlighted
chronic pain's enormous economic and personal burden and its recommendation for a national
pain strategy has led to today's meeting, which is being hosted by the Faculty of Pain
Medicine at the Australian and New Zealand College of Anaesthetists (ANZCA) with the
Australian Pain Society and Chronic Pain Australia. Professor Michael Cousins, Chair of
the steering committee for the meeting and Director of the Pain Management Research
Institute (PMRI), said chronic pain should be considered a disease in its own right and a
national health priority. "Everyone fears severe pain," explains Professor
Cousins, "Unfortunately, most of us will face some type of severe pain during our
lifetime and yet in 2009 an apparently simple problem such as the management of
"acute pain" – for example, after surgery or trauma - is still only
effectively managed in half of all patients, despite availability of knowledge and
techniques to provide effective treatment in 90% of patients.
How Coconut Oil Could Help Reduce
The Symptoms Of Type 2 Diabetes
A new study in animals demonstrates that a diet rich in coconut oil protects against
'insulin resistance' (an impaired ability of cells to respond to insulin) in muscle and
fat. The diet also avoids the accumulation of body fat caused by other high fat diets of
similar calorie content.
Potent tissue-specific effects of
medium chain fatty acids
MCFA reduce adiposity and preserve insulin action in muscle and adipose, despite inducing
steatosis and insulin resistance in the liver. Dietary supplementation with MCFA may
therefore be beneficial for preventing obesity and peripheral insulin resistance.
New links between epilepsy and
brain lipids
In mice that are missing a protein found only in the brain, neural signals "go
crazy," leaving the animals with epileptic seizures from a young age, researchers
have found. The report in the September 18th Cell, a Cell Press publication, details what
it is that happens when the protein encoded by plasticity related gene-1 (PRG-1) gets
lost, revealing an important fine-tuning mechanism for brain function. The researchers
show that PRG-1's usual calming influence in the brain depends on its proper interaction
with a particular class of lipids, known as lipid phosphates, which act as important
cellular signals. The team led by Robert Nitsch of Universitätsmedizin Berlin speculates
that changes in lipid phosphate signaling and PRG-1 function may be unrecognized causes of
epilepsy. Nitsch and his colleagues were the first to discover the new class of PRG
proteins and were particularly intrigued by PRG-1's peculiar pattern of activity; it
doesn't show up anywhere in the body or even anywhere else in the brain except on the
receiving ends of one type of neuron. "Most molecules are more or less found in most
cells," Nitsch explained. "Some are more confined, but only a very few are
confined to particular cell types in particular organs." In the new study they show
that PRG-1 deficient mice develop very severe seizures due to changes in brain activity.
Although the neural connections in the animals' brains appeared to be completely normal in
their structure, they showed they were far too excitable. When PRG-1 was restored to
individual neurons, activity levels returned to normal. That brain-tempering ability was
lost when a portion of PRG-1 that interacts with the lipid known as lysophosphatidic acid
(LPA) was altered. Animals lacking both PRG-1 and the LPA receptor didn't have epilepsy
either, more evidence that PRG-1 acts via the lipid signal. LPA has been known to play a
role in the brain and there were even some hints it could be involved in epilepsy, but
exactly what it does has remained unclear, Nitsch said. LPA is "sticky stuff that
goes into membranes," he said, not your everyday signaling molecule. LPA isn't itself
a neurotransmitter, but rather seems to fine-tune the release of glutamate, which is the
most prevalent of the chemical brain messengers, he explained. Without glutamate, brain
function would simply cease. LPA and its receptor operate on the sending side of neuronal
synapses. The new findings show that PRG-1 acts on the receiving side of synapses, taking
up LPA from the synapse to control the activity of the sending cell. (Synapses are the
small gaps between neurons where cell to cell communication takes place.) The findings add
a new layer to our understanding of how the brain functions.
Genes controlling insulin can alter
timing of biological clock
Many of the genes that regulate insulin also alter the timing of the circadian clock, a
new study has found. Although insulin responses were known to follow daily rhythms, the
finding that components of the insulin-control system can reset the body's clock surprised
the study's authors and suggests new approaches to treating disorders such as metabolic
syndrome that can result, at least in part, from chronic disruption of the sleep-wake
cycle. "People knew that the clock regulates many different processes, but what they
didn't realize what that when you tweak those processes, it feeds back and alters the
clock," said Steve Kay, Dean of the Division of Biological Sciences at the University
of California, San Diego, who led the study along with John Hogenesch of the University of
Pennsylvania. Several other important physiological control systems shift the clock as
well, they report online this week in the journal Cell. A molecular clock controls daily
physiological rhythms in many types of cells, even cells grown in culture. By engineering
cultured cells to glow yellow when a particular clock gene switched on, the team made the
cycle visible. They then interfered with every human gene to see which would shift the
clock. Hundreds altered the timing. "We just suddenly discovered 350 new genes that
affect the clock that weren't known before," Kay said. Subsequent screening to
confirm the genes' effect on a second clock gene narrowed the list to 200. Genes belonging
to four systems appeared on the "hit" list more often than chance would predict:
insulin and folate metabolism, and two systems that govern the life cycle and fate of
cells. Seven genes involved in insulin control also influenced the rhythms of the clock.
Guide on lung cancer in
'never-smokers'
A committee of scientists led by Johns Hopkins investigators has published a new guide to
the biology, diagnosis and treatment of lung cancer in never-smokers, fortifying measures
for what physicians have long known is a very different disease than in smokers. "It
is becoming increasingly clear that the genetic, cellular, and molecular nature of lung
cancer in many never-smokers is different from that of smoking-related lung cancers, and
there is good evidence now that the best treatment and prevention strategies for
never-smokers may be different as well," says Charles M. Rudin, M.D., Ph.D.,
associate director for Clinical Research at the Johns Hopkins Kimmel Cancer Center. Lung
cancer in never-smokers is the sixth leading cause of cancer-related deaths in the U.S.
Exposure to second-hand smoke and radon gas are thought to play important roles in causing
the disease in never-smokers. Radon, which leaks into homes from naturally occurring
uranium in soil, is known to be the leading cause of these cancers in U.S. populations,
but about half of never-smokers with lung cancer cannot be explained by known risk factors
identified in the guide, which also include asbestos, indoor wood-burning stoves, and
aerosolized oils caused by cooking. The guide, published as three papers in the September
15 issue of Clinical Cancer Research, resulted from a two-day meeting of 13 lung cancer
experts who convened at Johns Hopkins in 2007. The committee reviewed available evidence
from several hundred studies published by experts in public health, epidemiology,
molecular biology, pathology and oncology to identify distinctive characteristics of
never-smokers with lung cancer. Among the guide's recommendations is one calling on
organizers of lung cancer clinical trials to classify subjects by their smoking status and
evaluate outcomes accordingly. Committee members suggest that never-smokers should be
consistently defined as people who have smoked less than 100 cigarettes in their lifetime.
In absence of other democratic
institutions, freedom of press can lead to cycles of violence
While many have argued that media freedom is integral to a functioning democracy and
respect for human rights, a new study is the first to examine the effects of media freedom
in countries that lack such democratic institutions as fair elections. "We would
expect to find most free media in democratic states and most controlled media in
autocratic states, but this is not always the case," said Jenifer Whitten-Woodring, a
doctoral candidate in political science and international relations at USC. In the
September 2009 issue of International Studies Quarterly, Whitten-Woodring shows that media
freedom in autocratic states does not necessarily result in improved government treatment
of citizens. Indeed, media freedom in the absence of other institutional outlets for
dissent is actually associated with greater oppression of human rights, Whitten-Woodring
found utilizing data from 93 countries for the years 1981-1995. "The potential for
free news media to have a positive effect on government respect for human rights depends
on the presence of democratic institutions," Whitten-Woodring said. "Without
these characteristics, media freedom appears to have a negative impact on government
respect for human rights." Without democratic outlets for dissent, institutional
cycles of protest and repression are likely to evolve, according to Whitten-Woodring,
leading to the greater possibility of political imprisonment, murder, disappearance and
torture in the short term. For example in Iran in the late 1990s, when President Khatami
introduced some press freedom and newspapers began to report on violations of human
rights, protests and calls for reform were met with further repression.
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