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Week 38
Link between depression, early
stages of chronic kidney disease found by researchers
One in five patients with chronic kidney disease is depressed, even before beginning
long-term dialysis therapy or developing end-stage renal disease, UT Southwestern Medical
Center researchers have found. The study, based on a pool of 272 participants, is the
first to examine the rate of depression among these patients using the Diagnostic and
Statistical Manual of Mental Disorders 4th edition (DSM IV), which is considered the
gold-standard in evaluating depression. “Because patients in the early stages of
chronic kidney disease are at increased risk for clinical depression, we as nephrologists
should consider screening our patients for depression in clinic,” said Dr. Susan
Hedayati, assistant professor of internal medicine at UT Southwestern and a staff
nephrologist at the Dallas Veterans Affairs Medical Center. She is the lead author of the
study, available online and in the current issue of the American Journal of Kidney
Diseases.
Mayo Clinic researchers find lung
cancer oncogene holds key to turning off cancer stem cells
Scientists at the Mayo Clinic campus in Florida have found that the lung cancer oncogene
PKCiota is necessary for the proliferation of lung cancer stem cells. These stem cells are
rare and powerful master cells that manufacture the other cells that make up lung tumors
and are resistant to chemotherapy treatment. Their study, published in the Oct. 1 issue of
Cancer Research, also shows that an agent, aurothiomalate, being tested at Mayo Clinic in
a phase I clinical trial substantially inhibits growth of these cancer stem cells.
"Our data indicate that PKCiota is required for the earliest steps in the development
of lung cancer, which is the expansion of tumor-initiating cells or cancer stem
cells," says the study's senior author, Alan Fields, Ph.D., professor of pharmacology
in the College of Medicine, Mayo Clinic, and chair of the Department of Cancer Biology at
Mayo Clinic's campus in Florida.
Undergrad academic performance
linked to neural signals
Students will have to use their brains to get good grades at school this year, according
to new University of Toronto research that relates brain activity to undergraduate
academic performance. In the first study ever to link academic performance to a neural
signal, participants performed a Stroop task – a well-known test of cognitive control
– while hooked up to EEG electrodes that measured their brain activity. U of T
researchers monitored a brain signal known as the error-related negativity (ERN) in each
participant's brain while they completed the task. ERN signals are observed approximately
100 milliseconds after a mistake is made, and are involved in cognitive control and
self-regulation. Large ERN signals indicate a participant is responding strongly when
they've made a mistake; smaller ERN signals indicate they are less responsive to their
mistakes. The researchers then compared the size of each participant's ERN signals to
their official university transcript grades. "Those students with larger ERN signals
did significantly better in school, showing that these neural signals have important real
world implications," says doctoral researcher Jacob Hirsh. Hirsh says students with
large ERN signals are more responsive to their own errors than are students with smaller
ERNs. Those with large ERN signals are more likely to slow down in order to correct their
mistakes and avoid future errors, which could contribute to better grades. Because the
size of the ERN is only 50 per cent determined by genetics, though, Hirsh says students
may be able to improve their ERN signals by attending to their mistakes, thereby helping
to improve their academic performance. "The ERN is not set in stone," he says.
It's also key to note that having extremely large ERN signals is not ideal either, says
Dr. Michael Inzlicht, UofT Psychology Professor and co-author on the paper. "Students
with a small ERN may have more trouble in school, but people with a large ERN can suffer
from crippling anxiety because they respond strongly to the smallest perceived errors in
their own behaviour," says Inzlicht. "It all comes down to this: what is the
optimal response to an error?"
English slaughterhouses exposed. The public
is encouraged to believe that killing animals for their meat is essentially a pain- and
stress-free business so called humane slaughter. Film shot secretly in three
slaughterhouses between January and June 2009 by Animal Aid, exposes humane slaughter as a
sham. The footage is shocking and often deeply disturbing. For full background on the
investigation see www.animalaid.org.uk/
The film here is a 10 minute compilation of
footage from all three abattoirs.
Mercury In 1000s Of Foods
Containing High Fructose Corn Syrup
Stress, Cortisol & Health -
NICABM
Reduce Stress, Reduce Your
Waistline - Alvarado Hospital
With recessionary woes, more people are
under enormous stress. Stress is known to increase cortisol levels (stress hormone levels)
and, as a result, promotes weight gain. Dr. Larry Emdur of Alvarado Hospital talks about
how to reduce your stress levels and shrink your waistline.
Mapping Memory in the Brain
Eric R. Kandel, Howard Hughes Medical
Institute investigator, probes into the mind to demonstrate how it is much more complex
than just a series of processes carried out by the brain. The brain produces our every
emotional, intellectual and athletic act. It allows us to acquire new facts and skills,
and to remember them for as long as a lifetime. Memory exists in two major forms, each
located in different brain regions. Explicit memory is for people, places, and objects. In
contrast, implicit memory serves perceptual and motor skills. In concert, these two memory
systems help make us who we are.
Uighur Dilemma - China
Ever since the violence between Muslim
Uighurs and Han Chinese, a fear of fanaticism has taken hold. Is the government's decision
to demolish the Uighur area Kashgar really due to an earthquake threat? Kashgar is a
cultural icon. Parts of the city have stood for 2000 years and within its labyrinth,
Uighur traditions are unchanged. 'We live as we did in the old times' says Tursun, a 6
generation pot thrower. But times are changing. Beijing's deputy mayor has announced that
destruction of the old town is the only way to prepare for an earthquake threat. 'I spent
my whole childhood in this place. If they destroy it, we can't continue our business'
cries one of Kashgar's many blacksmiths. Many Uighur's are convinced that the authorities
'never tell the truth'. Yet some are happy to be rehoused in government buildings,
admitting that their homes are dangerous. Kashgar is of great strategic value for China -
if small separatist groups here link with Taliban insurgents across the border, there
could be a full-scale armed conflict in Western China. 'If a handful of religious
extremists, or international terrorists appear, we will crack down on them immediately'
says Beijing's deputy mayor. His plan could rebuild a sour relationship. Or give the
Uighurs a new reason to throw off Chinese occupation of their homeland.
The documentary focuses on the human rights
aspect of the Magdalene Laundries and shows how State and Church colluded to remand
and keep these women against their will. The film challenges the audience to look beyond
the historical significance of these institutions and most importantly, focuses on the
impact this experience had on the women in their daily lives once the laundries closed
down. It asks the important questions of why and how these institutions were allowed to
carry on until late 1996. It asks why these women never received a public apology or
redress from either State or Church. As young people living in Ireland, we believe it is
essential for this to be acknowledged equally with the industrial school, convent home,
orphanage and other environments of abuse
Autoimmune response can induce
pancreatic tumor rejection
Immune responses are capable of killing tumors before they can be directed toward normal
body tissue, according to new scientific findings published in Cancer Research, a journal
of the American Association for Cancer Research. "There are extremely precise
mechanistic methods augmenting the ability of the immune system to distinguish between
normal tissues and tumors," said lead researcher Richard G. Vile, Ph.D.
"Understanding the multiple checks and safeguards against autoimmunity should allow
us to understand more closely how to generate antitumor immunity." Vile, professor of
immunology in the Department of Molecular Medicine and the Department of Immunology at the
Mayo Clinic, Rochester, Minn., and professor of biological therapy at the University of
Leeds, United Kingdom, along with other colleagues, induced pathological damage to a
normal organ, in this case the pancreas, with the immune adjuvant hsp70. They investigated
whether that damage could lead to the development of T-cell responses against the normal
pancreas. Inflammatory killing of the normal pancreas induced a Th-1-like, anti-self
response to pancreatic antigens. Rapid suppression and damage to the pancreas induced a
very strong suppressive regulatory T-cell response — Treg. Even after Treg cells were
depleted, Vile and colleagues found that Th-1-like response was insufficient to induce
significant ongoing autoimmunity. "We believe that although there are additional
mechanisms that prevent autoimmunity, simply removing the Treg uncovered a good antitumor
response," Vile said. "We were not expecting that it would be possible to cure
tumors without autoimmunity. Our prediction was that we would have to generate potent
autoimmunity and then the tumors would be rejected." Based on this study, the
researchers suggested that it is more difficult than presumed to induce autoimmunity
against the pancreas because multiple immune safeguards exist to prevent potentially
autoimmune T-cells from destroying the normal pancreas. Further, when comparing the
immunoprotective mechanisms of different tissues, profound differences exist in response
to pathogen-like damage.
Prevent Periodontitis to Reduce the
Risk of Head and Neck Cancer
Chronic periodontitis, a form of gum disease, is an independent risk factor for head and
neck squamous cell carcinoma. This suggests the need for increased efforts to prevent and
treat periodontitis as a possible means to reduce the risk of this form of cancer.
"Prevent periodontitis; if you have it already, get treatment and maintain good oral
hygiene," said Mine Tezal, D.D.S., Ph.D., assistant professor in the Department of
Oral Diagnostic Sciences, School of Dental Medicine, University at Buffalo, and NYS Center
of Excellence in Bioinformatics and Life Sciences at the University of Buffalo. She is
also a research scientist in the Department of Dentistry and Maxillofacial Prosthetics at
Roswell Park Cancer Institute, which is where the study was conducted. Results of this
study are published in Cancer Epidemiology, Biomarkers & Prevention, a journal of the
American Association for Cancer Research. Chronic periodontitis is characterized by
progressive loss of the bone and soft tissue attachment that surround the teeth. The
researchers assessed the role of chronic periodontitis on head and neck squamous cell
carcinoma, as well as the individual roles on three subsites: oral cavity, oropharyngeal
and laryngeal. They used radiographic measurement of bone loss to measure periodontitis
among 463 patients; 207 of whom were controls. Findings showed that chronic periodontitis
might represent a clinical high-risk profile for head and neck squamous cell carcinoma.
The strength of the association was greatest in the oral cavity, followed by the
oropharynx and larynx, according to Tezal.
Seizure drug enhances sleep for
women with hot flashes
Gabapentin, a drug initially used to treat seizures, improves sleep quality in menopausal
women with hot flashes, University of Rochester Medical Center researchers report online
and in the September issue of the Journal of Women's Health.Approximately 40 percent of
menopausal women experience sleep disruption, often in the form of difficulty with sleep
initiation and frequent nighttime awakenings. The study is the first to show sustained
benefits in sleep quality from gabapentin, which Rochester researchers already have
demonstrated alleviates hot flashes. "Gabapentin improves sleep quality but does not
have the potential dependency problems of some other sleep medications and does not
involve the use of hormone replacement therapy," said Michael E. Yurcheshen, M.D.,
assistant professor of Neurology and the lead author of the article. "It has minimal
side effects and it is a generic drug," said Yurcheshen, who is based at the Strong
Sleep Disorders Center. "That makes it a very attractive treatment for these problems
in this patient population." For the current study, researchers used data from a
previously published randomized, double-blind, placebo-controlled trial of gabapentin in
59 postmenopausal women who experienced seven to 20 hot flashes daily. The subjects took
either 300 milligrams of gabapentin three times a day or a placebo. The research used a
factor analysis of the Pittsburgh Sleep Quality Index, a well-known and validated
questionnaire, to evaluate sleep. The results showed overall improvement in the sleep
quality score, even after 12 weeks of treatment.
Measuring nitrate concentrations in
leafy green vegetables
Leafy green vegetables such as lettuce, Asian greens, and spinach can accumulate high
concentrations of nitrate–nitrogen (NO3-N), which are potentially harmful if consumed
by humans. To measure NO3-N concentration in plant tissue, many laboratories use ion
selective electrodes (ISEs). Relatively inexpensive and portable ISE nutrient monitoring
devices, including the Cardy NO3-N meter, are widely used to measure fresh plant sap NO3-N
levels. Although conventional means of measuring plant tissue NO3-N are accurate and
reliable, they often require sophisticated equipment and trained technicians and can be
time-consuming, expensive, and impractical outside of a laboratory setting. A team of
researchers from Washington State University undertook a study to determine if rapid,
less-expensive tissue processing and analysis methods can substitute for more laborious,
expensive procedures to assess quality in leafy green vegetables. Scientists Kristy
Ott-Borrelli, Richard Koenig, and Carol Miles recently published the results of their
study that compared fresh sap expressed from whole leaves and analyzed with a Cardy meter
with the analysis of dry leaf tissue extracts analyzed with a benchtop ion selective
electrode and an automated colorimetric method for determining NO3-N concentration.
Ott-Borrelli explained the impetus for the study, stating; "It would be advantageous
for growers to have rapid and inexpensive methods to accurately measure plant tissue
NO3-N, allowing them to make fertility and harvest management decisions for these
crops." Samples for the study were taken from a larger experiment in which 24
varieties of lettuce, Asian greens, and spinach were harvested three times at two
locations during winter. Results from ISE and colorimetric analysis of the same dry leaf
tissue extracts had a strong relationship (r2 = 0.92). The ISE was relatively easy to
operate and affordable, suggesting it is an adequate substitute for automated colorimetric
analysis of dry plant tissue extracts.
Enzyme inhibitor takes an
unexpected approach toward blocking cancer-promoting protein
Scientists at Fox Chase Cancer Center have discovered a unique method of attack that may
be used to inhibit signaling enzymes called kinases, which often have a role in sustaining
drug-resistant cancerous cells. They have confirmed that IPA-3, a small molecular
inhibitor of a kinase called PAK1, targets the enzyme's regulatory domain, mimicking how
enzymes are naturally regulated within cells. "Typically, research has focused on
ways of blocking the active site of enzymes, the part of the enzyme that performs a
particular task," says Jeffrey R. Peterson, Ph.D, an assistant professor Fox Chase's
Cancer Genetics and Signaling program and co-author of the article. "The structure of
active site, however, is often shared among kinases, which makes it tough to target a
particular kinase without accidentally inhibiting a related enzyme." "By
targeting PAK1's specific regulatory domain, IPA-3 is highly selective molecule that takes
a more-or-less backdoor approach to shutting down a kinase, " Peterson says. "If
we can create drugs that take advantage of this mechanism, we could create new combination
therapies that will allow doctors to kill what might otherwise be drug-resistant
cells." Peterson and Julien Viaud, a postdoctoral researcher in the Peterson lab,
published their findings in the journal Molecular Cancer Therapeutics, available online
now. The researchers previously identified IPA-3 from a screen of 33,000 candidates, and
the molecule has since gone on to become an important subject of study by cancer
laboratories around the world. In the article, the researchers use a variety of techniques
to define how IPA-3 interacts with PAK1. "We found definitive proof that IPA-3 fit
into and binds to PAK1's autoregulatory domain, the part of the enzyme where it can,
essentially, shut itself off when necessary," Peterson says. "Our tests also
demonstrate that IPA-3 is highly selective for PAK1, which means that it is less likely it
will also turn off other kinases unintentionally."
Healthy older brains not
significantly smaller than younger brains, new imaging study shows
The belief that healthy older brains are substantially smaller than younger brains may
stem from studies that did not screen out people whose undetected, slowly developing brain
disease was killing off cells in key areas, according to new research. As a result,
previous findings may have overestimated atrophy and underestimated normal size for the
older brain. The new study tested participants in Holland's long-term Maastricht Aging
Study who were free of neurological problems such as dementia, Parkinson's disease or
stroke. Once participants were deemed otherwise healthy, they took neuropsychological
tests, including a screening test for dementia, at baseline and every three years
afterward for nine years. According to the report in the September Neuropsychology,
published by the American Psychological Association, participants were also given MRI
scans at Year 3 to measure seven different parts of the brain, including the memory-laden
hippocampus, the areas around it, and the frontal and cingulate areas of the cognitively
critical cortex. After examining behavioral data collected from 1994 to 2005 (with scans
taken between 1997 and 1999 depending on when people entered the study), the researchers
divided participants into two groups: one group with 35 cognitively healthy people who
stayed free of dementia (average starting age 69.1 years), and the other group with 30
people who showed substantial cognitive decline but were still dementia-free (average
starting age 69.2 years). That cognitive decline was measured by drops of at least 30
percent on two or more of six core tests of verbal learning and fluency, recall,
processing speed, and complex information processing, and/or drops of 3 or more points, or
scores of 24 or lower (raising suspicion for cognitive impairment), on the Mini-Mental
State Examination screening tool for dementia. In contrast to the 35 people who stayed
healthy, the 30 people who declined cognitively over nine years showed a significant
effect for age in the hippocampus and parahippocampal areas, and in the frontal and
cingulate cortices. In short, among the people whose cognition got worse, older
participants had smaller brain areas than younger participants.
'Hygiene hypothesis' challenged
New research hints that the common belief that kids who go to daycare have lower rates of
asthma and allergy later in life might be nothing more than wishful thinking. While young
children in daycare definitely do get more illnesses and experience more respiratory
symptoms as a result, any perceived protection these exposures afford against asthma and
allergy seem to disappear by the time the child hits the age of eight. "We found no
evidence for a protective or harmful effect of daycare on the development of asthma
symptoms, allergic sensitization, or airway hyper-responsiveness at the age of eight
years," wrote Johan C de Jongste, M.D., Ph.D., of Erasmus University in the
Netherlands and principle investigator of the study. "Early daycare was associated
with more airway symptoms until the age of four years, and only in children without older
siblings, with a transient decrease in symptoms between four and eight years." The
results are published in the September 15 issue of the American Journal of Respiratory and
Critical Care Medicine, a journal of the American Thoracic Society.The researchers
prospectively followed a birth cohort of nearly 4,000 Dutch children over the course of
eight years in the Prevention and Incidence of Asthma and Mite Allergy (PIAMA) Study.
Parents completed questionnaires during pregnancy, at three and 12 months, and then yearly
until the child reached the age of eight, and reported their children's airway symptoms
annually. At the age of eight, more than 3,500 of the children were also assessed for
specific allergies. Some also underwent testing for lung function and airway
hyper-responsiveness. Daycare use was assessed each year, and the children were
categorized in early attendees (first attendance before two years of age), late attendees
(first attendance between two and four years of age) and non-attendees. They found that
children who started daycare early were twice as likely to experience wheezing in the
first year of life compared to those who didn't go to daycare. However, as the children
aged, there was a shift: by age five, there was a trend for less wheezing among early
attendees: they were about 80 percent as likely as non-attendees to wheeze, but this was
not statistically significant. What's more, the shift reversed itself by age eight, when
there was no association between early daycare attendance and wheezing at all.
'Second hit' pushes noninvasive
breast cancer towards deadly metastasis
A new study identifies a molecule that acts cooperatively with a well known oncoprotein to
drive progression of noninvasive breast cancer to metastatic, life-threatening disease.
The research findings, published by Cell Press in the September issue of the journal
Cancer Cell, could have a significant impact on therapeutic decisions by facilitating
identification of high risk patients. Elevated ErbB2, a well known invasion and metastasis
promoting protein, is found in about one quarter of invasive breast cancers (IBC) and is
associated with poor patient survival. However, ErbB2 is also overexpressed in more than
half of noninvasive ductal carcinomas in situ (DCIS). DCIS, which is characterized by
proliferation of malignant cells within mammary ducts with no invasion into surrounding
tissues, is a precursor of IBC. It is not clear why ErbB2 is more frequently overexpressed
in noninvasive DCIS than in IBC or what drives the progression of DCIS to IBC. "For
effective reduction of cancer mortality, it is extremely important to predict the risk of,
and to intervene in, the critical transition from noninvasive DCIS to life-threatening
IBC," offers senior study author Dr. Dihua Yu from the Department of Molecular and
Cellular Oncology at the University of Texas, M. D. Anderson Center in Houston, Texas.
Previous research has led to the suggestion that additional risk factors may be needed for
the ErbB2-overexpressing DCIS to transition into IBC. Dr. Yu and colleagues examined
whether overexpression of 14-3-3?? a protein that belongs to a family of evolutionally
conserved proteins involved in cancer progression, could serve as a risk factor or
"second hit" and cooperate with ErbB2 to drive progression of DCIS to IBC. The
researchers observed that overexpression of both 14-3-3? and ErbB2 in DCIS was associated
with a higher risk of progressing to IBC. Elevated ErbB2 increased cell migration while
elevated 14-3-3? decreased cell adhesion, making it more likely that the malignant cells
could escape from the tissue structure. "Importantly, patients whose breast tumors
overexpressed both ErbB2 and 14-3-3? had higher rates of metastatic recurrence and death
than those whose tumors overexpressed only one," says Dr. Yu. The researchers went on
to identify pathways downstream of 14-3-3?, such as the TGF-?/Smads pathway, that may be
amenable to therapeutic intervention. "Our findings shed more light on the mechanism
of the deadly transition from non-invasive DCIS to the life-threatening invasive breast
cancer, in addition to solving a long time puzzle regarding breast cancers that
overexpress ErbB2. This study also identified biomarkers that allow selection of high-risk
DCIS patients for more aggressive treatments at early stages of cancer development, while
saving low-risk patients from ablative clinical procedures," offers Dr. Yu.
"Moreover, it provided promising targets for future intervention strategies to
prevent DCIS progression to IBC."
'Hygiene hypothesis' challenged
New research hints that the common belief that kids who go to daycare have lower rates of
asthma and allergy later in life might be nothing more than wishful thinking. While young
children in daycare definitely do get more illnesses and experience more respiratory
symptoms as a result, any perceived protection these exposures afford against asthma and
allergy seem to disappear by the time the child hits the age of eight. "We found no
evidence for a protective or harmful effect of daycare on the development of asthma
symptoms, allergic sensitization, or airway hyper-responsiveness at the age of eight
years," wrote Johan C de Jongste, M.D., Ph.D., of Erasmus University in the
Netherlands and principle investigator of the study. "Early daycare was associated
with more airway symptoms until the age of four years, and only in children without older
siblings, with a transient decrease in symptoms between four and eight years." The
results are published in the September 15 issue of the American Journal of Respiratory and
Critical Care Medicine, a journal of the American Thoracic Society.The researchers
prospectively followed a birth cohort of nearly 4,000 Dutch children over the course of
eight years in the Prevention and Incidence of Asthma and Mite Allergy (PIAMA) Study.
Parents completed questionnaires during pregnancy, at three and 12 months, and then yearly
until the child reached the age of eight, and reported their children's airway symptoms
annually. At the age of eight, more than 3,500 of the children were also assessed for
specific allergies. Some also underwent testing for lung function and airway
hyper-responsiveness. Daycare use was assessed each year, and the children were
categorized in early attendees (first attendance before two years of age), late attendees
(first attendance between two and four years of age) and non-attendees. They found that
children who started daycare early were twice as likely to experience wheezing in the
first year of life compared to those who didn't go to daycare. However, as the children
aged, there was a shift: by age five, there was a trend for less wheezing among early
attendees: they were about 80 percent as likely as non-attendees to wheeze, but this was
not statistically significant. What's more, the shift reversed itself by age eight, when
there was no association between early daycare attendance and wheezing at all.
'Second hit' pushes noninvasive
breast cancer towards deadly metastasis
A new study identifies a molecule that acts cooperatively with a well known oncoprotein to
drive progression of noninvasive breast cancer to metastatic, life-threatening disease.
The research findings, published by Cell Press in the September issue of the journal
Cancer Cell, could have a significant impact on therapeutic decisions by facilitating
identification of high risk patients. Elevated ErbB2, a well known invasion and metastasis
promoting protein, is found in about one quarter of invasive breast cancers (IBC) and is
associated with poor patient survival. However, ErbB2 is also overexpressed in more than
half of noninvasive ductal carcinomas in situ (DCIS). DCIS, which is characterized by
proliferation of malignant cells within mammary ducts with no invasion into surrounding
tissues, is a precursor of IBC. It is not clear why ErbB2 is more frequently overexpressed
in noninvasive DCIS than in IBC or what drives the progression of DCIS to IBC. "For
effective reduction of cancer mortality, it is extremely important to predict the risk of,
and to intervene in, the critical transition from noninvasive DCIS to life-threatening
IBC," offers senior study author Dr. Dihua Yu from the Department of Molecular and
Cellular Oncology at the University of Texas, M. D. Anderson Center in Houston, Texas.
Previous research has led to the suggestion that additional risk factors may be needed for
the ErbB2-overexpressing DCIS to transition into IBC. Dr. Yu and colleagues examined
whether overexpression of 14-3-3?? a protein that belongs to a family of evolutionally
conserved proteins involved in cancer progression, could serve as a risk factor or
"second hit" and cooperate with ErbB2 to drive progression of DCIS to IBC. The
researchers observed that overexpression of both 14-3-3? and ErbB2 in DCIS was associated
with a higher risk of progressing to IBC. Elevated ErbB2 increased cell migration while
elevated 14-3-3? decreased cell adhesion, making it more likely that the malignant cells
could escape from the tissue structure. "Importantly, patients whose breast tumors
overexpressed both ErbB2 and 14-3-3? had higher rates of metastatic recurrence and death
than those whose tumors overexpressed only one," says Dr. Yu. The researchers went on
to identify pathways downstream of 14-3-3?, such as the TGF-?/Smads pathway, that may be
amenable to therapeutic intervention. "Our findings shed more light on the mechanism
of the deadly transition from non-invasive DCIS to the life-threatening invasive breast
cancer, in addition to solving a long time puzzle regarding breast cancers that
overexpress ErbB2. This study also identified biomarkers that allow selection of high-risk
DCIS patients for more aggressive treatments at early stages of cancer development, while
saving low-risk patients from ablative clinical procedures," offers Dr. Yu.
"Moreover, it provided promising targets for future intervention strategies to
prevent DCIS progression to IBC."
Small molecule inhibits pathology
associated with myotonic dystrophy type 1
Researchers at the University of Illinois have designed a small molecule that blocks an
aberrant pathway associated with myotonic dystrophy type 1, the most common form of
muscular dystrophy. The new compound, soon to be tested in cells, binds tightly to its
target, an abnormally elongated RNA that hijacks part of the normal cellular machinery and
brings on symptoms of the disease. The newly developed compound is the first to show high
selectivity in binding the target while not disrupting other important RNA functions. The
study appears this week in the Proceedings of the National Academy of Sciences. Myotonic
dystrophy type 1, a muscle degeneration disease that so far is untreatable, affects about
one in 8,000 people worldwide. Some cases are mild, but others lead to a debilitating loss
of muscle control, declines in organ function and other potentially life-threatening
conditions. Scientists have recently identified a primary causative agent of the disease,
a mutant version of a gene, called DMPK, which contains an excessive number of
tri-nucleotide repeats. Nucleotides are the chemical letters that spell out the sequence
of a gene, and the normal version of the DMPK gene includes five to 34
cytosine-thymine-guanine (CTG) repeats. The mutant version of the gene includes 50 to as
many as 10,000 CTG repeats. "The longer the repeat the worse the disease and the
earlier the onset of the disease," said U. of I. chemistry professor and department
head Steven Zimmerman, who co-led the research with his colleague, chemistry professor
Anne Baranger. When the mutant DMPK is transcribed into RNA, the first step toward
building a protein, these (now CUG) repeats bind to a cellular protein, MBNL, which
normally splices other RNA transcripts. The bound MBNL cannot function properly, causing a
cascade of negative effects in the cell. Improperly spliced RNAs lead to improperly formed
proteins. Preventing the MBNL protein from binding to the CUG repeats has been shown to
ease the symptoms of the disease.
Nonagenarian researcher petitions
FDA to ban trans fats
Although Kummerow began publishing on trans fats in 1957, his efforts against trans fats
in food began in earnest in 1968, when he urged the American Heart Association to ask the
Institute of Shortening and Edible Oils to have its members decrease the amount of trans
fatty acids in shortenings and margarines, replacing them with essential fatty acids.
“Even then, there was strong evidence that trans fatty acids increased plasma
cholesterol levels,” Kummerow said.
Genomes reveal bacterial lifestyles
Sampling just a few genes can reveal not only the "lifestyle" of marine microbes
but of their entire environments, new research suggests. The finding means researchers may
be able to predict the types of microbes that thrive in specific marine environments by
sampling the genomes of just a few dominant species, according to research co-author Rick
Cavicchioli of the University of New South Wales. As well, it may reveal new insights into
the impacts of climate change on biodiversity in the world's oceans. "It's a bit like
using the DNA from a single hair at a crime scene to discover the identity of the
perpetrator," says Professor Cavicchioli. "What we've learned here is that a few
genes can tell us a much about the nature of the environment that species come from and
what influences them to evolve in a specific way." With other UNSW and US colleagues,
Professor Cavicchioli compared the genomes of two common ocean bacteria that employ
different strategies for living: one lives in nutrient-rich waters and is fast to grow and
replicate itself, and another lives in poor-nutrient waters, and grows more slowly. The
findings are published in the Proceedings of the National Academy of Sciences. The
comparison revealed genetic differences that reflect the different lifestyles of the two
species: the bacteria from the nutrient-rich waters have many selective transporter
proteins to quickly absorb plentiful nutrients while those from nutrient-poor waters have
a smaller number of highly efficient transporter proteins to extract what little nutrition
is available. Differences in other genes were also identified concerning nutrient and
energy usage and resistance to infecting viruses, which reflect the bacteria's adaptations
to their environment. Armed with such knowledge from a few key genes, it should be
possible to predict what sort of environment an individual species evolved in, says
Professor Cavicchioli. Better still, sampling the genomes of a small number of species
should enable scientists to gain useful new insights into the dynamics of whole marine
ecosystems.
Patterns of Life: Power of Habit
Dr. Richard Chopp on HIFU
EPA Fights FDA Bid To Ease Fish
Intake Limit Inside EPA
If the organic beansprouters are going to
BOYCOTT Whole Foods Market because its CEO stands for free market solutions to health care
problems, then we can BUYCOTT Whole Foods Market to show our SUPPORT for John Mackey, CEO.
Cell Phones give Brain Cancer
State of Play (2009)
Researchers find first evidence of
virus in malignant prostate cells
In a finding with potentially major implications for identifying a viral cause of prostate
cancer, researchers at the University of Utah and Columbia University medical schools have
reported that a type of virus known to cause leukemia and sarcomas in animals has been
found for the first time in malignant human prostate cancer cells. If further
investigation proves the virus, XMRV (Xenotropic murine leukemia virus-related virus),
causes prostate cancer in people, it would open opportunities for developing diagnostic
tests, vaccines, and therapies for treating the cancer, according to the study published
Sept. 7 online in the Proceedings of the National Academy of Sciences. Prostate cancer is
expected to strike nearly 200,000 U.S. males this year, making it the second most common
form of cancer, outside of skin cancers, among men."We found that XMRV was present in
27 percent of prostate cancers we examined and that it was associated with more aggressive
tumors," said Ila R. Singh, M.D., Ph.D., associate professor of pathology at
University of Utah and the study's senior author. "We still don't know that this
virus causes cancer in people, but that is an important question we're going to
investigate." Singh, also a member of the U of U's Huntsman Cancer Institute and
associate medical director at ARUP Laboratories, moved to Utah from Columbia University
Medical Center in 2008, where she began this research. She remains an adjunct faculty
member at Columbia. Along with providing the first proof that XMRV is present in malignant
cells, the study also confirmed that XMRV is a gammaretrovirus, a simple retrovirus first
isolated from prostate cancers in 2006 by researchers at the University of California, San
Francisco (UCSF), and the Cleveland Clinic. Gammaretroviruses are known to cause cancer in
animals, but have not been shown to do so in humans. The UCSF study did not examine benign
(non-malignant) prostate tissues, so could not link XMRV to prostate cancer. They also did
not find the virus in malignant cells.
Novel bacterial strains clear algal
toxins from drinking water
Novel bacterial strains capable of neutralizing toxins produced by blue-green algae have
been identified by researchers at Robert Gordon's University, Aberdeen. Aakash Welgama
presented the group's findings during the Society for General Microbiology's meeting at
Heriot-Watt University, Edinburgh. Blooms of blue green algae (cyanobacteria) are found in
both fresh and salt water throughout the world. They produce toxins called microcystins
which are released into the water and are easily ingested by animals and humans by
drinking, swimming or bathing in contaminated water. Once in the body the toxins attack
liver cells causing acute and chronic poisoning. Conventional methods for water treatment
such as sedimentation, sand filtration, flocculation and chlorination do not remove
microcystins. The researchers at Robert Gordon's University have identified more than ten
bacterial strains capable of metabolizing microcystins, breaking them down into harmless
non-toxic materials. The bacteria, Arthrobacter sp, Brevibacterium sp and Rhodococcus sp
were able to break down six commonly occurring microcystins. Six of the strains were
incubated in river water with variants of the toxin to simulate natural conditions; all
six strains were able to degrade the microcystins. The costs of advanced water
purification strategies are beyond most of the world's population," said Mr Welgama,
"Using bacteria to remove microcystins from water provides a reliable, cost-effective
purification system, which does not involve any use of harmful chemicals or any other
substances harmful to the environment".
How manuka honey helps fight
infection
Manuka honey may kill bacteria by destroying key bacterial proteins. Dr Rowena Jenkins and
colleagues from the University of Wales Institute - Cardiff investigated the mechanisms of
manuka honey action and found that its anti-bacterial properties were not due solely to
the sugars present in the honey. The work was presented this week (7-10 September), at the
Society for General Microbiology's meeting at Heriot-Watt University, Edinburgh.
Meticillin resistant Staphylococcus aureus (MRSA) was grown in the laboratory and treated
with and without manuka honey for four hours. The experiment was repeated with sugar syrup
to determine if the effects seen were due to sugar content in honey alone. The bacterial
cells were then broken and the proteins isolated and separated on a system that displayed
each protein as an individual spot. Many fewer proteins were seen from the manuka
honey-treated MRSA cells and one particular protein, FabI, seemed to be completely
missing. FabI is a protein that is needed for fatty acid biosynthesis. This essential
process supplies the bacteria with precursors for important cellular components such as
lipopolysaccarides and its cell wall. The absence of these proteins in honey-treated cells
could help explain the mode of action of manuka honey in killing MRSA. "Manuka and
other honeys have been known to have wound healing and anti-bacterial properties for some
time," said Dr Jenkins, "But the way in which they act is still not known. If we
can discover exactly how manuka honey inhibits MRSA it could be used more frequently as a
first-line treatment for infections with bacteria that are resistant to many currently
available antibiotics".
Piece from childhood virus may save
soldiers' lives
A harmless shard from the shell of a common childhood virus may halt a biological process
that kills a significant percentage of battlefield casualties, heart attack victims and
oxygen-deprived newborns, according to research presented Sunday, September 6, 2009, at
the 12th European meeting on complement in human disease in Budapest, Hungary. Introducing
the virus's shell in vitro shuts down what's known as the complement response, a
primordial part of the immune system that attacks and destroys the organs and vascular
lining of people who have been deprived of oxygen for prolonged periods, according to
researchers at Children's Hospital of The King's Daughters (CHKD) and Eastern Virginia
Medical School (EVMS), in Norfolk, Va. The complement response kicks in after the victim
has been revived, in what is known as a reperfusion injury. It does its work slowly but
unrelentingly, killing soldiers, infants or heart attack victims over the course of days.
"To find a way to manipulate the complement system pharmacologically has been like a
search for the Holy Grail," said one of the lead researchers, Dr. Kenji Cunnion, an
infectious disease physician at CHKD and an associate professor of pediatrics at EVMS.
While Cunnion and Neel Krishna, Ph.D., a pediatric virologist at CHKD and assistant
professor of microbiology at EVMS, focus on pediatric research, they see clear military
applications. "The complement reaction is one of the major causes of death of the
battlefield," said Krishna. "By the time you get a victim to the hospital, it
may be too late."
Fear of insurance rejection deters
potentially life saving genetic tests for bowel cancer
An Australian study of families with genetic risk of bowel cancer has found that 50
percent of participants declined genetic testing when informed of insurance implications.
"This indicates that people have a significant fear of insurance discrimination which
impacts their decision to have potentially life saving genetic testing," says co-lead
author Dr Louise Keogh, of the University of Melbourne's Key Centre for Women's Health in
Society. The population-based study was led by researchers from the University of
Melbourne and the Cancer Council Victoria, and published in the prestigious Medical
Journal of Australia today. Researchers identified 106 people from 25 families in which
there were genetic mutations that increase the risk of bowel cancer. All were offered the
chance to learn their own individual genetic information at a Familial Cancer Clinic.
"When we told participants about the life insurance implications of genetic testing,
the number declining genetic testing more than doubled from 20 per cent to 50 per
cent," Dr Keogh said. "In Australia, while genetic information has no
implications for health insurance, it can affect life, trauma, disability and sickness and
accident insurance policies, "says co-lead author Christine van Vliet, School of
Medical Sciences, University of New South Wales. "However this is not the case in all
countries. Since we know all people have some genes which predispose to disease, it is
important that the Australian life insurance industry does not deter people from learning
about their genetic risks," she says. Bowel cancer is the second most common cancer
for men and women in Australia. One in every 3,000 Australians carry a genetic mutation
that places them at high risk of bowel cancer.
Smoke no longer found in European
hospitals
Tobacco use is prohibited in hospitals in many European countries, although levels of
compliance with this regulation differ. A study carried out by researchers from the
Catalan Institute of Oncology (ICO) has shown for the first time that exposure to
environmental tobacco smoke in European hospitals is "low", and "without
any notable differences" between them. Europe wants to see smoking in all closed
public places banned by 2012. However, to date only 10 European countries – Spain is
not among them – are applying this regulation comprehensively. Now a research study
has described the levels of environmental tobacco smoke in European hospitals and has
shown for the first time that exposure is "low" and "without any notable
differences between them". The study, carried out in 2001 in 30 hospitals throughout
seven European countries (Germany, Austria, Belgium, France, Greece, Romania and Spain)
measured levels of particulates with a diameter of 2.5 micros (known as PM2.5) (?g/m3) or
below, which indicate the presence of environmental tobacco smoke, at six standard sites
in each hospital. Esteve Fernández, lead author of the study and a researcher at the ICO,
tells SINC "it is important to measure compliance with laws by regularly measuring
levels of environmental tobacco smoke". To do this, the experts suggest that national
and European regulations to control tobacco addiction should ban smoking in health
establishments without any exceptions. In total, 199 PM2.5 measurements were taken, 30 of
them in the vestibules of main hospital entrances, 29 in casualty department waiting
rooms, 22 in medical hospitalisation units, 27 in cafeterias, 22 on fire escape stairways,
22 in general surgery hospitalisation units, and 39 in other places, including eight
smokers' areas (in Belgium and Greece).
Discovery leads to rapid mouse
'personalized trials' in breast cancer
One person's breast cancer is not the same as another person's, because the gene mutations
differ in each tumor. That makes it difficult to match the best therapy with the
individual patient. Using a finding that the genetic complexity of tumors in mice
parallels that in humans, researchers at the Duke University Institute for Genome Sciences
and Policy and Duke University Medical Center are starting trial studies in mice, just
like human clinical trials, to evaluate whether understanding tumor diversity can improve
cancer treatment. "Giving everyone the same few current treatments doesn't take the
very different types of tumors into account," said Joseph Nevins, Ph.D., Barbara
Levine University Professor of Breast Cancer Genomics at Duke, who directs the Center for
Applied Genomics & Technology at Duke. "It's like trying to treat a virus
infection without recognizing that it may be HIV, influenza or cold virus." For a
study appearing this week in the Proceedings of the National Academy of Sciences, Nevins
and colleagues painstakingly examined a large number of mouse breast tumors and performed
genomic analyses to differentiate the tumors. "The genetic pathways in the tumors
determine the sensitivity to drugs," Nevins said. "We still have so much to
learn about this." All of the mice were bred to have a Myc gene variant that gave
them tumors; however, additional gene mutations are acquired that contribute to the
development of the tumor, including mutations in the Ras gene and others. The spectrum of
tumor variation at the genetic level mimicked the complexity of human cancers. "If we
are going to successfully treat a tumor, we must recognize the extensive heterogeneity of
what we call breast cancer and match drugs carefully to the characteristics of that
particular tumor," Nevins said. "Today breast tumors may be sorted by whether
they are estrogen-sensitive or HER-2 sensitive, but that is about the extent of it. We are
performing human trials to look at the underlying biological pathways and examine how best
to match therapies with the individual patient. But, these are lengthy studies. Now we can
develop new strategies to match a therapy with a mouse tumor subtype and have results in a
much shorter period of time."
Researchers identify key
contributor to pre-eclampsia
A new study by researchers at Wake Forest University School of Medicine reveals a key
component in the development of preeclampsia in pregnant women, a condition that can
result in miscarriage and maternal death.The study, funded by the National Institutes of
Health, appears in the September issue of Endocrinology. In it, researchers focused on
identifying the differences in the uteri of pregnant women with and without preeclampsia
and how the mother's tissues vary from the immediately adjacent fetus' tissue in
preeclamptic women. "Preeclampsia is a very serious condition that affects 7 to 10
percent of all pregnancies in the United States," said K. Bridget Brosnihan, Ph.D.,
the lead investigator for the study and a professor in the Hypertension and Vascular
Research Center at the School of Medicine. "It can be devastating to both mother and
baby, and currently there is no cure except to deliver the fetus. Our finding brings us
one step closer to understanding the condition by getting a picture of what is happening
at the maternal and fetal interface." Preeclampsia is a disorder that occurs only
during pregnancy and the postpartum period. It is a rapidly progressive condition that
impacts multiple body systems, causing high blood pressure, decreased liver function and,
in the most severe cases, affecting the activity of the brain, resulting in seizures.
Swelling, sudden weight gain, headaches and changes in vision are among the symptoms;
however, some women with rapidly advancing disease report few symptoms. Left untreated,
preeclampsia can lead to serious, even fatal, complications for both mother and baby. The
condition contributes significantly to neonatal morbidity and mortality and is the second
leading cause of maternal death. By conservative estimates, preeclampsia and other
hypertensive disorders during pregnancy are responsible for 76,000 maternal and 500,000
infant deaths each year, according to the Preeclampsia Foundation. Despite numerous
research studies, the specific causes of preeclampsia remain a mystery. One possible
pathway that has been identified is the renin-angiotensin system (RAS), which regulates
blood pressure and fluid retention.
New research strategy for
understanding drug resistance in leukemia
UCSF researchers have developed a new approach to identify specific genes that influence
how cancer cells respond to drugs and how they become resistant. This strategy, which
involves producing diverse genetic mutations that result in leukemia and associating
specific mutations with treatment outcomes, will enable researchers to better understand
how drug resistance occurs in leukemia and other cancers, and has important long-term
implications for the development of more effective therapies. “In trying to
understand why certain cancers respond to drugs while certain other cancers fail to
respond, we found that a single gene can be the culprit for drug resistance,” said
Kevin Shannon, MD, senior author of the paper and a pediatric cancer specialist at UCSF
Children’s Hospital. “The subtlety of what makes a cancer cell become resistant
to a drug is truly remarkable.”
Syracuse University research team
discovers switch that causes the body to produce cancerous cells
A team of Syracuse University researchers discovered a second molecular switch within the
Mixed Lineage Leukemia protein complex that they believe could be exploited to prevent the
overproduction of abnormal cells that are found in several types of cancer, including
leukemia. The paper was designated as the "Paper of the Week" in the September 4
issue of the Journal of Biological Chemistry (JBC), published by the American Society for
Biochemistry and Molecular Biology. Only the top 1 percent of the more than 6,600 articles
published each year in JBC receives this prestigious designation. The research team is led
by biologist Michael Cosgrove, assistant professor in SU's College of Arts and Sciences.
Anamika Patel, a post-doctoral researcher in Cosgrove's lab, who is being featured on
JBC's website, did much of the experimental work for the paper. During the course of their
research to better understand MLL, a protein switch that helps regulate the formation of
white blood cells, Cosgrove's research group discovered a new molecular switch within the
MLL complex, which they labeled W-RAD. "We thought that MLL was the only switching
mechanism present in this protein complex," Cosgrove said. "However, we
discovered the complex is really two switches." In normal cells, MLL combines with
four proteins that comprise the W-RAD group to create a molecular switch that controls DNA
packaging events required to form white blood cells. When the MLL switch is broken, white
blood cells do not mature properly, resulting in a dangerous proliferation of abnormal
cells.
Cardiac biomarker levels strongly
predict outcome of bypass surgery
Levels of a biomarker used in the diagnosis of heart attacks are almost universally
elevated in patients who have undergone coronary-artery bypass grafting (CABG) and, when
markedly elevated, are powerfully prognostic, a team of researchers from the Massachusetts
General Hospital (MGH) Heart Center has found. Their report implies that, while
measurement of cardiac troponin T (cTnT) can help determine patient prognosis, current
consensus recommendations regarding the use of cTNT to diagnosis post-CABG heart attack
(myocardial infarction) probably should be reconsidered. The paper appears in the
September 8 issue of Circulation and has been released online,"Although postoperative
concentrations of cTnT were powerfully predictive of the risk of complications and death
after CABG, we found the currently recommended cut-points for diagnosing myocardial
infarction are far too low," says James Januzzi, MD, director of the MGH Cardiac
Intensive Care Unit, the study's senior author. "But use of cTnT to predict overall
postoperative risk does look very promising." Patients recovering from bypass
surgery, in which blood supply to the heart muscle is rerouted around one or more blocked
coronary arteries, are at risk for a number of postoperative complications, including
heart attack. Current standards for the diagnosis of post-operative myocardial infarction
include consideration of symptoms such as chest pain, electrocardiogram changes and the
results of biomarker tests. However, since patients recovering from cardiac surgery
inevitably experience chest pain and the results of postoperative electrocardiograms are
often unclear, clinicians may heavily rely on biomarkers like cTnT to diagnose post-CABG
heart attacks. An earlier study of the prognostic role of cTnT in cardiac surgery patients
found that extreme elevations of the enzyme strongly predicted the risk of complications
and death in the year following surgery. But that study examined a mixture of
post-cardiac-surgery patients and also did not consider diagnostic guidelines outlined in
a 2007 consensus statement from four organizations, including the American Heart
Association and the American College of Cardiology. The current study was designed to
specifically evaluate the usefulness of cTnT in the diagnosis of post-CABG heart attack
and to examine factors associated with postoperative cTnT elevation and how well cTnT
levels predicted postoperative complications in general. Measurements of cTnT levels were
taken from almost 850 CABG patients immediately after their procedures and 6, 8, 18 and 24
hours later. Those levels were then analyzed based on several factors related to the
patients' original illness, surgery, and short- and long-term outcomes.
U of T researchers identify protein
Researchers at the University of Toronto have identified a protein which plays a key role
in the development of neurons, which could enhance our understanding of how the brain
works, and how diseases such as Alzheimer's occur. U of T graduate student John Calarco,
working in the labs of Prof. Ben Blencowe (Donnelly Centre for Cellular and Biomolecular
Research, University of Toronto) and Prof. Mei Zhen (Samuel Lunenfeld Research Institute,
Mount Sinai Hospital), has identified a protein known as nSR100, which is only found in
vertebrate species and which controls a network of "alternative splicing events"
that are located in the messages of genes with critical functions in the formation of the
nervous system. The findings are published in a paper in the current edition of the
journal Cell. Alternative splicing events greatly expand the diversity of the genetic
messages and corresponding proteins produced by genes in vertebrate cells, and this
process partially accounts for the evolution of remarkable complexity in organs such as
the mammalian brain. Calarco, recipient of a prestigious Alexander Graham Bell
Studentship, together with colleagues in the Blencowe Lab, identified nSR100 using
computational and experimental methods and then determined its role in the control of
alternative splicing in the brain. These studies revealed that nSR100 regulates splicing
events in genes that help form neurons. Collaborator and co-author Brian Ciruna and his
colleagues at the the Hospital for Sick Children (SickKids) in Torontofurther demonstrated
that nSR100 plays a critical role in the development of the vertebrate nervous system.
"The brain is by far the most complex organ in the human body and understanding how
it functions represents one of the foremost challenges of biomedical research. A large
number of neurological disorders arise when the development and function of certain
neurons is impaired. A major research goal is therefore to identify key genes required for
the specification and function of neurons in the brain, and nSR100 represents such a
gene," said Prof. Blencowe, principal investigator on the study.
Anticancer compound found in
American mayapple
A common weed called American mayapple may soon offer an alternative to an Asian cousin
that's been harvested almost to extinction because of its anti-cancer properties. The
near-extinct Asian plant, Podophyllyum emodi, produces podophyllotoxin, a compound used in
manufacturing etoposide, the active ingredient in a drug used for treating lung and
testicular cancer. Podophyllyum emodi is a cousin of the common mayapple weed found in the
United States. Podophyllotoxin is found in Indian mayapple (Podophyllum emodii Wall.),
American mayapple (Podophyllum peltatum L.), and other species. Podophyllotoxin and its
derivatives are used in several commercially available pharmaceutical products such as the
anticancer drugs etoposide, teniposide, and etopophos, which are used in the treatment of
small-cell lung cancer, lymphoblastic leukemia, testicular cancer, and brain tumors.
Podophyllotixin derivatives are also used for the treatment of psoriasis and malaria, and
some are being tested for the treatment of rheumatoid arthritis. Currently,
podophyllotoxin is produced commercially using the roots and rhizomes of Indian mayapple,
an endangered species harvested from the wild in India, Pakistan, Nepal, and China.
Researchers at Mississippi State University and the University of Mississippi recently set
out to identify American mayapple types with high podophyllotoxin content. Valtcho D.
Zheljazkov and colleagues at Mississippi State University published the research results
in HortScience. According to Zheljazkov; "The objective of this study was to estimate
podophyllotoxin concentration in American mayapple across its natural habitats in the
eastern United States and to identify high podophyllotoxin types that could be used for
further selection and cultivar development." Mayapple has been long been grown as a
cash crop in Europe and Russia, but has never been introduced or domesticated in the
United States, although the idea was suggested by researchers more than 30 years ago.
Previous research demonstrated that American mayapple leaves contain podophyllotoxin,
making way for the development of American mayapple as a high-value crop for American
growers. Zheljazkov explained that, until now, there has been no comprehensive study on
the genetic resources of American mayapple colonies across the United States. "We
hypothesized that there might be great variation with respect to podophyllotoxin content
within American mayapple across the eastern United States."
MicroRNAs circulating in blood show
promise as biomarkers to detect pancreatic cancer
A blood test for small molecules abnormally expressed in pancreatic cancer may be a
promising route to early detection of the disease, researchers at The University of Texas
M. D. Anderson Cancer Center report in the September edition of the journal Cancer
Prevention Research. The team's analysis of four microRNAs (miRNA) found in the blood
plasma of pancreatic cancer patients is proof of principle to further develop a blood test
for this evasive disease, said senior author Subrata Sen, Ph.D., associate professor in M.
D. Anderson's Department of Molecular Pathology. "Increased expression of microRNAs
is known to be involved with specific genetic pathways and processes responsible for the
development of cancer-associated changes in cells," Sen said. "Detection of
elevated levels of miRNAs in blood plasma of pancreatic cancer patients as informative
biomrkers of disease appears to be a promising, novel approach for developing a minimally
invasive assay for detecting this disease."There is no accurate, noninvasive way to
detect pancreatic cancer, the fourth-leading cause of cancer-related deaths in the United
States. Fewer than 5 percent of patients survive to five years. MicroRNAs are
single-stranded bits of RNA consisting of 18 to 24 nucleotides that regulate the messenger
RNA (mRNA) expressed by genes to tell a cell's protein-making machinery what protein to
make. The four targeted microRNAs previously had been associated in varied ways with
pancreatic cancer or with precancerous lesions. Expression of the four was analyzed in 28
patients with pancreatic cancer and 19 healthy people. The four combined markers
accurately identified 64 percent (sensitivity) of the pancreatic cancer cases and
correctly identified 89 percent of those without disease (specificity). That degree of
sensitivity and specificity are good for a pilot study but don't yet rise to the levels
required for translation in the clinic, which would require investigating more circulating
microRNAs in blood in a larger sample of persons representing different stages of the
disease and healthy controls.
Scripps research scientists
identify genetic cause for type of deafness
A team led by scientists from The Scripps Research Institute has discovered a genetic
cause of progressive hearing loss. The findings will help scientists better understand the
nature of age-related decline in hearing and may lead to new therapies to prevent or treat
the condition. The findings were published the September 3, 2009, in an advance, online
issue of the American Journal of Human Genetics, a publication of Cell Press. "It is
thought that mutations in several hundred genes can lead to deafness," said team
leader Ulrich Mueller, a professor in the Department of Cell Biology and member of the
Skaggs Institute for Chemical Biology at Scripps Research. "However, for many forms
of deafness, we don't know what effects the genes have. In this new research, we have
linked a previously uncharacterized gene to deafness, first in mice and then in
humans." The team found that the gene responsible for the hearing loss—called
Loxhd1—is necessary for maintaining proper functioning hair cells in the inner ear.
Mutations in Loxhd1 lead to degradation of the hair cells and a disruption of the process
that enables hearing.
Scripps Research Scientists
Illuminate Structure of Circulating Lung Cancer Cells
Most cancer-related deaths are caused by metastases—the spread of cancer to other
parts of the body—and tumor cells that circulate in the bloodstream are generally
understood to be the cause of these dangerous secondary tumors. Now, for the first time, a
collaboration led by scientists from The Scripps Research Institute has been able to
determine the structural features of circulating tumor cells, which were collected from
the blood of a woman with advanced lung cancer. The ability to detect and characterize
these cells may provide new insight into their metastatic potential, and could also result
in advances in the diagnosis, treatment, and management of the disease. The study, which
was conducted in collaboration with members of the Scripps Clinic, The Palo Alto Research
Center, and the Billings Clinic (Montana), was published as the cover article in the
September 2009 edition (Vol 133, Issue 9) of the journal Archives of Pathology and
Laboratory Medicine, a major clinical journal published by the College of American
Pathologists. "This study is a breakthrough," said team leader Peter Kuhn, a
Scripps Research associate professor in the department of Cell Biology. "We were able
to find these cells and image them so clearly that they can be used as clinical biopsy
material. We didn't just count them—we were able to interpret them."
That late-night snack - worse than
you think
Eat less, exercise more. Now there is new evidence to support adding another
"must" to the weight-loss mantra - eat at the right time of day. A Northwestern
University study has found that eating at irregular times -- the equivalent of the middle
of the night for humans, when the body wants to sleep -- influences weight gain. The
regulation of energy by the body's circadian rhythms may play a significant role. The
study is the first causal evidence linking meal timing and increased weight gain.
"How or why a person gains weight is very complicated, but it clearly is not just
calories in and calories out," said Fred Turek, professor of neurobiology and
physiology in the Weinberg College of Arts and Sciences and director of the Center for
Sleep and Circadian Biology. "We think some factors are under circadian control.
Better timing of meals, which would require a change in behavior, could be a critical
element in slowing the ever-increasing incidence of obesity." The findings could have
implications for developing strategies to combat obesity in humans, as the United States
and the world battle what has been called an "obesity epidemic." More than 300
million adults worldwide are obese, including more than a third of American adults.
Details of the obesity study, which was led by Turek, will be published online Sept. 3 by
the journal Obesity. "One of our research interests is shift workers, who tend to be
overweight," said lead author Deanna M. Arble, a doctoral student in Turek's lab.
"Their schedules force them to eat at times that conflict with their natural body
rhythms. This was one piece of evidence that got us thinking -- eating at the wrong time
of day might be contributing to weight gain. So we started our investigation with this
experiment."
U-M researchers find gene that
protects high-fat-diet mice from obesity
University of Michigan researchers have identified a gene that acts as a master switch to
control obesity in mice. When the switch is turned off, even high-fat-diet mice remain
thin. Deleting the gene, called IKKE, also appears to protect mice against conditions
that, in humans, lead to Type 2 diabetes, which is associated with obesity and is on the
rise among Americans, including children and adolescents. If follow-up studies show that
IKKE is tied to obesity in humans, the gene and the protein it makes will be prime targets
for the development of drugs to treat obesity, diabetes and complications associated with
those disorders, said Alan Saltiel, the Mary Sue Coleman Director of the U-M Life Sciences
Institute. "We've studied other genes associated with obesity – we call them
'obesogenes' – but this is the first one we've found that, when deleted, stops the
animal from gaining weight," said Saltiel, senior author of a paper to be published
in the Sept. 4 edition of the journal Cell. "The fact that you can disrupt all the
effects of a high-fat diet by deleting this one gene in mice is pretty interesting and
surprising," he said. Obesity is associated with a state of chronic, low-grade
inflammation that leads to insulin resistance, which is usually the first step in the
development of Type 2 diabetes. In the Cell paper, Saltiel and his colleagues show that
deleting, or "knocking out," the IKKE gene not only protected high-fat-diet mice
from obesity, it prevented chronic inflammation, a fatty liver and insulin resistance, as
well. The high-fat-diet mice were fed a lard-like substance with 45 percent of its
calories from fat. Control mice were fed standard chow with 4.5 percent of its calories
from fat. The dietary regimen began when the mice were 8 weeks old and continued for 14 to
16 weeks.
Mice can eat 'junk' and not get fat
A study in the September 4th issue of the journal Cell, a Cell Press publication,
identifies a gene that springs into action in response to a high fat diet. Mice that lack
the gene become essentially immune to growing obese, regardless of their eating habits.
The protein encoded by the gene known as I?B kinase e (IKKe) belongs to a class of
enzymes, the kinases, which typically make for good drug targets because they are
relatively easy to block, according to the researchers. Even better in terms of its
therapeutic promise, IKKe loss seems to have many beneficial effects. Mice without the
gene are protected against weight gain, chronic inflammation, fatty liver and insulin
resistance. "Perhaps most interestingly, the mice burn more calories even though they
aren't eating any less or exercising more," said Alan Saltiel of the University of
Michigan, Ann Arbor. They apparently keep the weight off on a diet loaded with fat by
"producing a little heat." Loss of the gene seems to release the
"brakes" on energy expenditure, Saltiel adds. In the beginning, his team did not
expect IKKe to have such far-reaching effects on obesity. Growing evidence has linked the
insulin resistance in obesity to a state of chronic, low-grade inflammation. Saltiel's
group suspected that IKKe had a role in eliciting that inflammatory state. Earlier studies
have found that if you stop the inflammatory chain of events in obesity, you can break the
link between obesity and diabetes, Saltiel said. In the current study, "we expected
to disrupt that link, but instead we stopped the onset of obesity." Further analysis
of gene activity within mice lacking IKKe offered more clues to its influence. Loss of the
gene reduces the expression of inflammatory cytokines, along with certain regulatory
proteins and enzymes involved in glucose and lipid metabolism. The researchers suspect
that IKKe's effects involve the interplay between the liver, fat and immune response in
obesity. It may not play a role in the initial inflammatory response to a high-fat diet,
but might be required for sustaining that state, they say.
Newly discovered road map of leptin
explains its regulation of bone and appetite
New research from Columbia University Medical Center has illuminated a previously unknown
leptin-serotonin pathway in the brain that simultaneously promotes appetite and bone mass
accrual. The research, which explains how leptin – well-known appetite-suppressing
hormone – acts in the brain, is published in the Sept. 4 issue of Cell. When the
leptin-serotonin pathway is turned on in mice, the researchers found, appetite increases,
the animals eat more, gain weight, and their bone mass increases. When the pathway is
turned off, mice eat less, lose weight, and their bones weaken. Furthermore, leptin was
found to not act in the hypothalamus as previously thought, but in the brain stem acting
on serotonin, a hormone that in the brain acts to control appetite, mood and anger. The
identification of this pathway helps explain why, as doctors have long known, obese people
tend to have a significantly lower prevalence of osteoporosis, says the study's senior
author, Gerard Karsenty, M.D., Ph.D., chair of the Department of Genetics &
Development at Columbia University's College of Physician and Surgeons. Though obese
people produce high levels of leptin, they are resistant, or unresponsive, to its signals
– instead, they operate in a false state of leptin deficiency, which increases
serotonin – and thereby, appetite and bone mass. Dr. Karsenty points out that these
current findings may have more influence on developing a new way to reduce appetite and
obesity than preventing osteoporosis. "It will be difficult to turn on the pathway to
strengthen bone without increasing appetite at the same time," Dr. Karsenty said.
"But this finding shows that it is feasible to alter parts of the leptin-serotonin
pathway to decrease appetite without weakening bone."
