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Week 30
Einstein Scientists Link Elevated
Insulin to Increased Breast Cancer Risk
Elevated insulin levels in the blood appear to raise the risk of breast cancer in
postmenopausal women, according to researchers at Albert Einstein College of Medicine of
Yeshiva University. Their findings are published in the online version of the
International Journal of Cancer.Increased breast cancer risk for postmenopausal women has
previously been linked to obesity and diabetes. Both conditions involve insulin
resistance, which causes increases in circulating levels of insulin. Since insulin is
known to promote cell division and enhance breast tumor growth in animal models, the
Einstein scientists reasoned that relatively high insulin levels may contribute to breast
cancer risk in women. "Up to now, only a few studies have directly investigated
whether insulin levels are associated with breast cancer risk, and those studies have
yielded conflicting results," says Geoffrey Kabat, Ph.D., senior epidemiologist in
the department of epidemiology and population health at Einstein and the lead author of
the paper. "Those other studies were based on just a single baseline measurement of
insulin, while our study involved analyzing repeated measurements of insulin taken over
several years — which provides a more accurate picture of the possible association
between insulin levels and breast cancer risk."
Diets bad for the teeth are also
bad for the body
Dental disease may be a wake-up call that your diet is harming your body. "The
five-alarm fire bell of a tooth ache is difficult to ignore," says Dr. Philippe P.
Hujoel, professor of dental public health sciences at the University of Washington (UW)
School of Dentistry in Seattle. Beyond the immediate distress, dental pain may portend
future medical problems. It may be a warning that the high-glycemic diet that led to
dental problems in the short term may, in the long term, lead to potentially serious
chronic diseases. Hujoel reviewed the relationships between diet, dental disease, and
chronic systemic illness in a report published July 1 in the Journal of Dental Research.
He weighed two contradictory viewpoints on the role of dietary carbohydrates in health and
disease. The debate surrounds fermentable carbohydates: foods that turn into simple sugars
in the mouth. Fermentable carbohydrates are not just sweets like cookies, doughnuts, cake
and candy. They also include bananas and several tropical fruits, sticky fruits like
raisins and other dried fruits, and starchy foods like potatoes, refined wheat flour,
yams, rice, pasta, pretzels, bread, and corn. One viewpoint is that certain fermentable
carbohydrates are beneficial to general health and that the harmful dental consequences of
such a diet should be managed by the tools found in the oral hygiene section of
drugstores. A contrasting viewpoint suggests that fermentable carbohydrates are bad for
both dental and general health, and that both dental and general health need to be
maintained by restricting fermentable carbohydrates. The differing perspectives on the
perceived role of dietary carbohydrates have resulted in opposing approaches to dental
disease prevention, Hujoel notes, and have prompted debates in interpreting the link
between dental diseases and such systemic diseases as obesity, diabetes, and some forms of
cancer. Over the past twenty years or so, Hujoel says, people have been advised to make
fermentable dietary carbohydrates the foundation of their diet. Fats were considered the
evil food. A high-carbohydrate diet was assumed to prevent a number of systemic chronic
diseases. Unfortunately, such a diet - allegedly good for systemic health - was bad for
dental health. As a result, cavities or gingival bleeding from fermentable carbohydrates
could be avoided only – and not always successfully, as Hujoel points out -- by
conscientious brushing, fluorides, and other types of dental preventive measures. When
these measures are not successful, people end up with cavities and gum disease.
Spread your sperm the smart way
Attractive males release fewer sperm per mating to maximise their chances of producing
offspring across a range of females, according to a new paper on the evolution of
ejaculation strategies. The findings by researchers at UCL (University College London) and
the University of Oxford suggest that, paradoxically, matings with attractive males may be
less fertile than those with unattractive ones. In a paper to be published in the journal
American Naturalist, the team mathematically modelled a range of male ejaculation
strategies to look for the optimum “sperm load” per mating, and how this might
vary depending on mating patterns. Previous studies have shown that in animals such as the
domestic fowl, and fish such as the Arctic charr, males with privileged access to females
produce ejaculates of lower fertilising quality than subordinate males. Sam Tazzyman, UCL
CoMPLEX (Centre for Mathematics and Physics in the Life Sciences and Experimental
Biology), says: “In some species, females mate with many different males. Each
male’s sperm competes with that of other males in a process known as ‘sperm
competition’. Since males have finite resources to allocate to breeding, they
allocate them carefully to each mating to maximise their number of offspring. If a male
puts a lot of resources into each mating he will get more offspring per mating, but at the
expense of fewer matings. If, on the other hand, a male puts few resources into each
mating he will secure less paternity per mating, but will be able to carry out more
matings overall. Thus, there is a trade-off between number of matings and success per
mating." “How a male negotiates this trade-off depends on how easy he finds it
to attract females. The more attractive a male is, the more females will be willing to
mate with him, reducing the value of each mating to him. This means it is optimal for him
to contribute fewer sperm per mating. Although this reduces fertility per mating, it
maximises the number of offspring he sires overall. Less attractive males secure fewer
matings but value each of them more highly, and by allocating more sperm to each mating
make the most of their meagre opportunities. This leads to the rather paradoxical
prediction that matings with attractive males may be less fertile than those with
unattractive males."
Finnish study identifies factors
that increase death in stroke patients ages 15 to 49
Heavy drinking, being 45 to 49 years old, type 1 diabetes or having a preceding infection
are associated with more than twice the risk of death in stroke patients 15 to 49 years
old, according to a Finnish study.Furthermore, heart failure was associated with seven
times the risk of death and active cancer malignancy with 16 times the risk of death in
stroke patients. The overall death rate is low in this age group, said Jukka Putaala,
M.D., who led the study. Risk of death was 2.7 percent at one month, 4.7 percent at one
year and 10.7 percent at five years with no difference based on gender. Detecting these
factors associated with higher risk of death is important because they can be modified by
lifestyle changes, strictly controlled medication or medical procedures in most patients,
Putaala said.
Caltech chemists say antibody
surrogates are just a 'click' away
Chemists at the California Institute of Technology (Caltech) and the Scripps Research
Institute have developed an innovative technique to create cheap but highly stable
chemicals that have the potential to take the place of the antibodies used in many
standard medical diagnostic tests. James R. Heath, the Elizabeth W. Gilloon Professor and
professor of chemistry, along with K. Barry Sharpless, the W. M. Keck Professor of
Chemistry at the Scripps Research Institute and winner of the 2001 Nobel Prize in
Chemistry, and their colleagues, describe the new technique in the latest issue of
Angewandte Chemie, the leading European journal of chemistry.Last year, Heath and his
colleagues announced the development of the Integrated Blood-Barcode Chip, a diagnostic
medical device, about the size of a microscope slide, which can separate and analyze
dozens of proteins using just a pinprick of blood. The barcode chip employed antibodies,
proteins utilized by the immune system to identify, bind to, and remove particular foreign
compounds, such as bacteria and viruses—or other proteins. "The thing that
limits us in being able to go to, say, 200 proteins in the barcode chip is that the
antibodies that you use to detect the proteins are unstable and expensive," says
Heath. "We have been frustrated with antibodies for a long time, so what we wanted to
be able to do was develop antibody equivalents—what we call 'protein capture
agents'—that can bind to a particular protein with very high affinity and
selectivity, and that pass the following test: you put a powder of them in your car trunk
in August in Pasadena, and you come back a year later and they still work." In the
new work, Heath and his colleagues, including Caltech graduate student Heather D. Agnew,
the first author on the Angewandte paper, have developed a protocol to quickly and cheaply
make such highly stable compounds, which are composed of short chains of amino acids, or
peptides. "I actually traveled to Chicago with a vial of my capture agents as airline
carry-on luggage, and came back with it, and the reagent still worked," says Agnew.
The technique makes use of the "in situ click chemistry" method, introduced by
Sharpless in 2001, in which chemicals are created by joining—or
"clicking"—smaller subunits together.
Map of your brain may reveal early
mental illness
John Csernansky wants to take your measurements. Not the circumference of your chest,
waist and hips. No, this doctor wants to stretch a tape measure around your hippocampus,
thalamus and prefrontal cortex. OK, maybe not literally a tape measure, but he does want
to chart the dimensions of the many structures in the human brain. From those measurements
-- obtained from an MRI scan -- Csernansky will produce a map of the unique dips, swells
and crevasses of the brains of individuals that he hopes will provide the first scientific
tool for early and more definite diagnosis of mental disorders such as schizophrenia.
Diagnosing the beginning stage of mental disorders remains elusive, although this when
they are most treatable. The shapes and measurements of brain structures can reveal how
they function. Thus, Csernansky hopes his brain maps will reveal how the brains of humans
with and without major mental disorders differ from each other and the time frame over
which those differences develop. Diagnosing psychiatric disorders currently is more art
than science, said Csernansky, M.D., the chair of psychiatry and behavioral sciences at
the Northwestern University Feinberg School of Medicine and of psychiatry at the Stone
Institute of Psychiatry at Northwestern Memorial Hospital. Unlike a heart attack, for
example, which can be identified with an EKG and a blood test for cardiac enzymes,
psychiatric illness is diagnosed by asking a patient about his symptoms and history.
"That's akin to diagnosing a heart attack by asking people when their pain came and
where it was located," Csernansky said. "We would like to have the same kinds of
tools that every other field of medicine has." To that end, he is heading a National
Institutes of Mental Health study to measure the differences between the structure of the
schizophrenic and normal brain to be able to more quickly identify schizophrenia in its
early stages and see if the medications used to treat the illness halt its devastating
advance. Schizophrenia usually starts in the late teens or early 20s and affects about 1
percent of the population. If the disease is caught early and treated with the most
effective antipsychotic medications and psychotherapy, the patient has the best chance for
recovery.
‘Normal’ Cells Far from
Cancer Give Nanosignals of Trouble
A new Northwestern University-led study of human colon, pancreatic and lung cells is the
first to report that cancer cells and their non-cancerous cell neighbors, although quite
different under the microscope, share very similar structural abnormalities on the
nanoscale level. The findings, obtained using an optical technique that can detect
features as small as 20 nanometers, validate the “field effect,” a biological
phenomenon in which cells located some distance from a malignant or premalignant tumor
undergo molecular and other kinds of abnormal changes. The most striking findings were
that these nanoscale alterations occurred at some distance from the tumor and,
importantly, could be identified by assessing more easily accessible tissue, such as the
cheek for lung cancer detection. The partial wave spectroscopy (PWS) technique, once
optimized, could be used to detect cell abnormalities early and help physicians assess who
might be at risk for developing cancer. Like a pap smear of the cervix, a simple brushing
of cells is all that is needed to get the specimen required for testing.
Tuna Fishing - South Pacific - BBC
Two
Episode 6 Fragile Paradise: The South
Pacific is still relatively healthy and teeming with fish, but it is a fragile paradise.
International fishing fleets are taking a serious toll on the sharks, albatross and tuna,
and there are other insidious threats to these bountiful seas. This episode looks at what
is being done to preserve the ocean and its wildlife.
Welcome to the new BBC Earth
channel on YouTube
The people of Nigeria versus Shell
Friends of the Earth Netherlands, her
Nigerian sister organisation ERA and four Nigerian farmers and fishermen claim that Royal
Dutch Shell is liable for the damage oil spills have caused in the villages of Nigerian
people. Because a Dutch company with an annual profit of 27 billion dollars cannot ignore
the responsibility for the consequences of its actions.
Confidence in scientists on the
decline
Barely six out of ten Swedes have confidence in scientists and there has been a decline of
six percentage points over the past year. Supporters of the Left Party and the Nationalist
Democrats (political parties at each end of the political spectrum) have the least
positive view of scientific development, according to a new study carried out by Vetenskap
& Allmänhet (Public & Science), VA, and the SOM Institute 58 per cent of Swedes
have a high or fairly high level of confidence in scientists, compared to 62 per cent last
year and a full 67 per cent six years ago when this survey was first carried out.
Professors Sören Holmberg and Lennart Weibull of the SOM Institute believe that the
financial crisis may have contributed to the decline in confidence. “A lot of
attention has been focused on how poorly experts and researchers have understood the
situation, and on their inability to predict what happened.”
Molecules with a higher selective
ability to exterminate cancer cells
Researchers of the Department of Pharmaceutical Chemistry of the University of Granada
(UGR), led by Joaquín Campos Rosa, have obtained a new type of molecules which have
proven -in in vitro cultivations- a high level of efficiency against cancer cells, as well
as very low toxicity against the body's normal cells. This important discovery in the
cancer therapy field is the result of a Project of Excellence of the Andalusian Ministry
of Innovation, Science and Enterprise in its first call, funded with 102,400 euros. This
discovery, which was made possible thanks to natural substances never used before for the
treatment of tumours, is the result of modifying the chemical structure of a very used
drug against cancer - 5-fluoruracile, one of the first drugs used in Oncology, by another
similar substance called uracile. Uracile is a substance that is naturally present in our
body, which is part of the cells' RNA. After the good results obtained with uracile, this
substance was replaced by other similar molecules, but even more effective (guanine and
cytosine). With them, the new molecules have been obtained, whose main feature is a higher
therapeutical rate, that is, the quotient between the affectation over cancer cells and
that over healthy cells. More specifically, their toxicity for the body is ten times lower
than that of 5-fluoruracile. The efficiency of the molecules obtained is related to their
high capacity to induce apoptosis in cancer cells. Apoptosis is a function of the body
that consists of programming the oldest cells' death, as they are no longer useful. Just
like new cells are constantly born in our tissues, the oldest ones must also gradually die
as they no longer carry out their function properly. Therefore apoptosis is a mechanism of
defence of the body as it also takes place in those cells that are a threat due to
failures in their normal activity. When the capability of a cell to carry out the
apoptosis is damaged (for example due to a mutation) or if the beginning of apoptosis has
been blocked (by a virus), the damaged cell can keep on splitting without any major
restriction, thus giving rise to a tumour that can be carcinogen.
Baylor researchers unravel mystery
of DNA conformation
DNA appears a perfect spring that can be stretched and then spring back to its original
conformation. How far can you stretch it before something happens to the structure and it
cannot bounce back? What happens when it is exposed to normal cellular stresses involved
in doing its job? That was the problem that Zechiedrich and her colleagues tackled. Their
results also addresses a question posed by another Nobel laureate, the late Dr. Linus
Pauling, who asked how the information encoded by the bases could be read if it is
sequestered inside the DNA molecular with phosphate molecules on the outside. It's easy to
explain when the cell divides because the double-stranded DNA also divides at the behest
of a special enzyme, making its genetic code readily readable. "Many cellular
activities, however, do not involve the separation of the two strands of DNA," said
Zechiedrich. To unravel the problem, former graduate student, Dr. Graham L. Randall,
mentored jointly by Zechiedrich and Dr. B. Montgomery Pettitt
(http://www.chem.uh.edu/Faculty/Pettitt/Research/) of UH, simulated 19 independent DNA
systems with fixed degrees of underwinding or overwinding, using a special computer
analysis started by Petttitt. They found that when DNA is underwound in the same manner
that you might underwind a spring, the forces induce one of two bases – adenine or
thymine – to "flip out" of the sequence, thus relieving the stress that the
molecule experiences. "It always happens in the underwound state," said
Zechiedrich. "We wanted to know if torsional stress was the force that accounted for
the base flipping that others have seen occur, but for which we had no idea where the
energy was supplied to do this very big job." When the base flips out, it relieves
the stress on the DNA, which then relaxes the rest of the DNA not involved in the base
flipping back to its "perfect spring" state.
Tobacco smoke can trigger child's
asthma attack
Exposure to smoke can worsen your child's asthma and should be eliminated to help
effectively manage symptoms, said a pediatric pulmonologist at Baylor College of Medicine.
"Sometimes treating a child's asthma means treating the parent's tobacco
addiction," said Dr. Harold Farber, associate professor of pediatrics - pulmonary at
BCM and associate medical director of the Texas Children's Health Plan at Texas Children's
Hospital."Cigarette smoke – in first-, second- and third-hand forms – poses
a serious threat to your child's asthma. It's the first thing we look at when starting a
management program for controlling asthma." When children with asthma are exposed to
smoke, medications don't work as well and flare-ups or attacks can be more severe, Farber
said. "The most important thing that a parent who smokes can do for their child with
asthma is to get treatment for their own tobacco addiction," he said.
Research Shows Prescribers Miss
Possibly Dangerous Drug Interactions
Research led by The University of Arizona College of Pharmacy has found that medication
prescribers correctly identified fewer than half of drug pairs with potentially dangerous
drug-drug interactions. These findings raise concern because of the high number of drugs
Americans take: an average of 2.3 medications is prescribed during each physician office
visit. A synopsis of the research was published in May Research Activities, a digest of
research findings intended to contribute to the national policymaking process. The
researchers, led by Daniel Malone, PhD, professor at the UA College of Pharmacy, mailed a
questionnaire to 12,500 U.S. prescribers who were selected based on a history of
prescribing drugs associated with known potential for drug-drug interaction. Prescribers
were primarily physicians, physicians’ assistants and nurse practitioners. Recipients
were asked to classify 14 drug pairs as “contraindicated,” “may be used
together but with monitoring” or “no interaction.” Respondents could also
state that they were “not sure.”
Asian Spice Could Reduce Breast
Cancer Risk in Postmenopausal Women Exposed to Hormone Replacement Therapy, MU Study Finds
Previous studies have found that postmenopausal women who have taken a combined estrogen
and progestin hormone replacement therapy have increased their risk of developing
progestin-accelerated breast tumors. Now, University of Missouri researchers have found
that curcumin, a popular Indian spice derived from the turmeric root, could reduce the
cancer risk for women after exposure to hormone replacement therapy. "Approximately 6
million women in the United States use hormone replacement therapy to treat the symptoms
of menopause," said Salman Hyder, the Zalk Endowed Professorship in Tumor
Angiogenesis and professor of biomedical sciences in the College of Veterinary Medicine
and the Dalton Cardiovascular Research Center. "This exposure to progestin will
predispose a large number of post-menopausal women to future development of breast cancer.
The results of our study show that women could potentially take curcumin to protect
themselves from developing progestin-accelerated tumors."
Hush Little Baby... Linking Genes,
Brain, and Behavior in Children
It comes as no surprise that some babies are more difficult to soothe than others but
frustrated parents may be relieved to know that this is not necessarily an indication of
their parenting skills. According to a new report in Psychological Science, a journal of
the Association for Psychological Science, children's temperament may be due in part to a
combination of a certain gene and a specific pattern of brain activity. The pattern of
brain activity in the frontal cortex of the brain has been associated with various types
of temperament in children. For example, infants who have more activity in the left
frontal cortex are characterized as temperamentally "easy" and are easily calmed
down. Conversely, infants with greater activity in the right half of the frontal cortex
are temperamentally "negative" and are easily distressed and more difficult to
soothe. In this study, Louis Schmidt from McMaster University and his colleagues
investigated the interaction between brain activity and the DRD4 gene to see if it
predicted children's temperament. In a number of previous studies, the longer version (or
allele) of this gene had been linked to increased sensory responsiveness, risk-seeking
behavior, and attention problems in children. In the present study, brain activity was
measured in 9-month-old infants via electroencephalography (EEG) recordings. When the
children were 48 months old, their mothers completed questionnaires regarding their
behavior and DNA samples were taken from the children for analysis of the DRD4 gene.
Research identifies successful new
treatment for Hodgkin's lymphoma, reduces long-term risks
New research led by Cindy Schwartz, MD, of Hasbro Children's Hospital has identified a new
chemotherapy regimen for pediatric Hodgkin lymphoma (HL) patients. The new treatment
enhances efficacy through dose-dense drug delivery while simultaneously reducing the
long-term risks presented by high cumulative dose chemotherapy. Schwartz and the
researchers of the Children's Oncology Group have published their findings in the journal
Blood (posted in an online first edition). The Children's Oncology Group's Hodgkin
Lymphoma Committee, led by Schwartz, director of pediatric hematology/oncology at Hasbro
Children's Hospital, recognized that treatment for HL in the United States was not being
treated with the most modern treatment models, in large part because it was one of the
first malignancies for which a curative chemotherapy regimen was developed. Schwartz says,
"For decades, the chemotherapy regimens known as MOPP and ABVD had been the standard
treatment options for these patients. However, while they yielded excellent survival
rates, they often resulted in long-term effects from toxicity, including infertility,
second malignancy and cardiopulmonary toxicity. With the new treatment paradigm we've
developed, in essence, we've been able to cure the cancer while reducing the risk of
long-term effects on our patients." The group designed a new chemotherapy treatment
known as ABVE-PC, combining six different drugs into one "dose-dense" regimen
that could limit the cumulative doses of each drug below the recognized thresholds known
for resulting in long-term toxicity. Their goal was to reach a rapid early response (RER)
in order to further reduce cumulative therapy and to thereby increase event-free survival
(EFS). They also combined the chemotherapy treatment with low dose radiation following the
completion of the ABVE-PC cycles. The treatment developed by the researchers was unique
given that its focus was on early response after nine weeks, measuring to detect primary
chemosensitivity – a favorable response to chemotherapy, indicating that the therapy
is working. This approach differs from the traditional evaluation of the response at the
end of chemotherapy. Schwartz notes that this is important, because, "This early
detection allows for a reduction in therapy for those who respond well to the dose-dense
treatment, and therefore, individual response can be tailored for maximum efficacy."
Schwartz, who is also a professor of pediatrics at The Warren Alpert Medical School of
Brown University, believes that the study represents a new treatment model for patients
with HL. She states, "Our treatment paradigm for advanced HL relied on two treatment
principles: dose density enhances therapeutic efficacy and rapid early response is
evidence of chemosensitivity and can serve as a basis for reduction of therapy."
UCLA scientists identify how immune
cells may help predict Alzheimer's risk
What if you could test your risk for Alzheimer's disease much like your cholesterol levels
— through a simple blood test? UCLA scientists have discovered a way to measure the
amount of amyloid beta that is being absorbed by immune cells in the blood. Amyloid beta
forms the plaques considered the hallmark of Alzheimer's disease, and if the immune system
isn't adequately clearing amyloid beta, it may indicate Alzheimer's risk, according to the
researchers. MP Biomedicals LLC, a global life sciences and diagnostics company dedicated
to Alzheimer's disease research, has received an exclusive, worldwide license to
commercialize the UCLA technology and create a diagnostic blood test for public use to
screen for Alzheimer's risk. "Early diagnosis is the cornerstone of preventive
approaches to Alzheimer's disease," said Dr. Milan Fiala, lead author of the UCLA
study and a researcher at the David Geffen School of Medicine at UCLA and the Veterans
Affairs Greater Los Angeles Healthcare System. "We are pleased that the process we've
identified using immune cells to help predict Alzheimer's risk will be further developed
by MP Biomedicals." "We are excited by the opportunity to forward the UCLA
science in creating a cost-effective blood test to screen for Alzheimer's risk that could
be used in any hospital or lab," said Milan Panic, CEO of MP Biomedicals. Dr. Miodrag
Micic, vice president of research and development for MP Biomedicals, noted that other
blood tests for Alzheimer's diagnosis measure factors such as inflammation and infection,
which are also present in other diseases like atheroclerosis and may complicate the
interpretation of results.
Probiotics help gastric-bypass
patients lose weight more quickly, Stanford study shows
New research from the Stanford University School of Medicine and Stanford Hospital &
Clinics suggests that the use of a dietary supplement after Roux-en-Y gastric bypass
surgery can help obese patients to more quickly lose weight and to avoid deficiency of a
critical B vitamin.In a study published in the July issue of the Journal of
Gastrointestinal Surgery, John Morton, MD, associate professor of surgery at the medical
school, showed that patients who take probiotics after the gastric-bypass procedure tend
to shed more pounds than those who don't take the supplements. Probiotics are the
so-called "good" bacteria found in yogurt as well as in over-the-counter dietary
supplements that help in the digestion of food. "Surprisingly, the probiotic group
attained a significantly greater percent of excess weight loss than that of control
group," said Morton, who wrote the paper with lead author Gavitt Woodard, a
third-year medical student, and five other medical students at the Surgery Center for
Outcomes Research and Evaluation in Stanford's Department of Surgery. Morton has performed
more than 1,000 of these bypasses at Stanford Hospital & Clinics. The researchers
followed 44 patients on whom Morton had performed the procedure from 2006 to 2007.
Patients were randomized into either a probiotic or a control group. Both groups received
the same bariatric medical care and nutritional counseling, as well as the support of
weight-loss study groups. Both groups also were allowed to consume yogurt, a natural
source of probiotics. In addition, the probiotic group consumed one pill per day of
Puritan's Pride, a probiotic supplement that is available online and in many stores.
Morton has no financial ties to the company that makes the supplement.The study showed
that at three months, the probiotics group registered a 47.6 percent weight loss, compared
with a 38.5 percent for the control group. The study also found that levels of vitamin
B-12 were higher in the patients taking probiotics — a significant finding because
patients often are deficient in B-12 after gastric-bypass surgery. The probiotics group
had B-12 levels of 1,214 picograms per milliliter at three months, compared with the
control group's levels of 811 pg/mL.
Study finds citrus-derived
flavonoid prevents obesity
A flavonoid derived from citrus fruit has shown tremendous promise for preventing weight
gain and other signs of metabolic syndrome which can lead to Type 2 Diabetes and increased
risk of cardiovascular disease. The study, led by Murray Huff of the Robarts Research
Institute at The University of Western Ontario looked at a flavonoid (plant-based
bioactive molecule) called naringenin. The findings are published online in the journal
Diabetes. In the study one group of mice was fed a high-fat (western) diet to induce the
symptoms of metabolic syndrome. A second group was fed the exact same diet and treated
with naringenin. Naringenin corrected the elevations in triglyceride and cholesterol,
prevented the development of insulin resistance and completely normalized glucose
metabolism. The researchers found it worked by genetically reprogramming the liver to burn
up excess fat, rather than store it. "Furthermore, the marked obesity that develops
in these mice was completely prevented by naringenin," says Huff, Director of the
Vascular Biology Research Group at Robarts and Professor of Medicine and Biochemistry at
the Schulich School of Medicine & Dentistry. "What was unique about the study was
that the effects were independent of caloric intake, meaning the mice ate exactly the same
amount of food and the same amount of fat. There was no suppression of appetite or
decreased food intake, which are often the basis of strategies to reduce weight gain and
its metabolic consequences." While grapefruit has long been linked to weight loss
diets, the concentrations of the citrus-derived flavonoid being studied are at higher
levels than you could get from dietary components. "We are examining the
pharmacological properties of naringenin," explains Huff. "The next step is to
find out if naringenin prevents heart disease in animal models and to explore the
feasibility of clinical trials to determine its safety and efficacy in humans." This
study investigated naringenin's preventative properties, but Huff is also investigating
whether it can treat obesity and other existing metabolic problems. "These studies
show naringenin, through its insulin-like properties, corrects many of the metabolic
disturbances linked to insulin resistance and represents a promising therapeutic approach
for metabolic syndrome."
Living a Nightmare: Animal
Factories in Michigan
A 24-minute documentary about the horrors
of industrial agriculture in Michigan.
Generation Kill - Iraq
What happens when those who've grown up on
Hollywood war movies and graphic video games are sent to the frontline? "It's the
ultimate rush -- you're going into the fight with a good song playing in the
background," states one soldier. This is a war fought by the first playstation
generation. As Rolling Stones journalist Evan Wright explains: "One thing about them
is they kill very well in Iraq."
With Gaza devoid of medical care, the
critically ill must travel to Israel. There they are asked to comply with Israeli
intelligence before treatment. Become a hated informer? Or refuse and wait to die?
With Gaza blockaded, only a fortunate few are able to get through Erez crossing, the only
passenger crossing that remains between Gaza and Israel. It took 6 months to secure a
permit for my daughter says Majed, whose daughter needs an urgent operation. Even after
securing a permit the struggle isnt over. Once in Israel, desperate and weak patients like
27 year old Khitam are often subjected to rigorous cross-examination. When I finally went
in I was interrogated for 2 hours Khitam says, they asked me about the resistance, gave me
a pen and paper and asked for names. Since the war, Israeli intelligence has used
Palestinian informers to target militant leaders, especially those involved in Hamas. When
Khitam told the intelligence that she didnt know anything, that shed spent the last 9
months lying in a hospital bed, they accused her of being involved in Hamas and sent her
back to Gaza. I will die, thats it. Theres nothing else I can do she says frankly. Khitam
has no choice, but with the threat of Palestinian wrath hanging over becoming an informer,
more and more Palestinians are opting to die.
If that office inkjet printer has become just another fixture, it's time to take a fresh
look at it. Similar technology may soon be used to develop paper-based biosensors that can
detect certain harmful toxins that can cause food poisoning or be used as bioterrorism
agents. In a paper published in the July issue of Analytical Chemistry, John Brennan and
his research team at McMaster University, working with the Sentinel Bioactive Paper
Network, describe a method for printing a toxin-detecting biosensor on paper using a
FujiFilm Dimatix Materials Printer. The researchers demonstrated the concept on the
detection of acetylcholinesterase (AChE) inhibitors such as paraoxon and aflatoxin B1 on
paper using a "lateral flow" sensing approach similar to that used in a home
pregnancy test strip. The process involves formulating an ink like the one found in
computer printer cartridges but with special additives to make the ink biocompatible. An
ink comprised of biocompatible silica nanoparticles is first deposited on paper, followed
by a second ink containing the enzyme, and the resulting bio-ink forms a thin film of
enzyme that is entrapped in the silica on paper. When the enzyme is exposed to a toxin,
reporter molecules in the ink change colour in a manner that is dependent on the
concentration of the toxin in the sample. This simple and cost-effective method of
adhering biochemical reagents to paper is expected to bring the concept of bioactive paper
a significant step closer to commercialization. The goal for bioactive paper is to provide
a rapid, portable, disposable and inexpensive way of detecting harmful substances,
including toxins, pathogens and viruses, without the need for sophisticated
instrumentation. The research showed that the printed enzyme retains full activity for at
least two months when stored properly, suggesting that such sensor strips should have a
good shelf life.
Building memories with actin
Memories aren't made of actin filaments. But their assembly is crucial for long-term
potentiation (LTP), an increase in synapse sensitivity that researchers think helps to lay
down memories. In the July 13, 2009 issue of the Journal of Cell Biology (www.jcb.org),
Rex et al. reveal that LTP's actin reorganization occurs in two stages that are controlled
by different pathways, a discovery that helps explain why it is easy to encode new
memories but hard to hold onto them. If you can't seem to forget those ABBA lyrics you
heard in seventh grade but can't remember Lincoln's Gettysburg address, the vagaries of
LTP might be to blame. Neuroscientists think that the process, in which a brain synapse
becomes more potent after repeated stimulation, underlies the formation and stabilization
of new memories. LTP involves changes in the anatomy of synapses and dendritic spines, a
process that depends on reorganization of the supporting actin cytoskeleton. However,
researchers didn't know what controlled these changes. Rex et al. tackled the question by
dosing slices of rat hippocampus with adenosine, a naturally occurring signal that
squelches LTP. Adenosine prevents phosphorylation and inactivation of cofilin, an
inhibitor of actin filament assembly, the team found. Cofilin's involvement, in turn,
implicates signaling cascades headed by GTPases, such as the RhoA-ROCK and Rac-PAK
pathways. The researchers showed that a ROCK inhibitor stalled actin polymerization and
resulted in a short-lived LTP. A Rac-blocking compound had no effect.
Childhood obesity link to parents
Like father, like son -- new research points to gender relationships between parents and
their children as vital factor in childhood obesity. The relationships between children
and their parent of the same gender in the earliest years of life could be the key to
understanding why some young people become obese and others do not, new research conducted
by the EarlyBird Diabetes Study has shown. A study published today in the International
Journal of Obesity indicates that girls whose mothers are classified as clinically obese
are significantly more likely to struggle with weight problems in childhood, with a
similar relationship existing between obese fathers and their sons. The findings showed
that the same trend does not exist between mothers and their sons and fathers and their
daughters – meaning that behavioural, rather than genetic, factors could be the key
to unravelling the causes of the current obesity epidemic affecting children in the UK.
Novel drug discovery tool could
identify promising new therapies for Parkinson's disease
Researchers funded by the National Institutes of Health have turned simple baker's yeast
into a virtual army of medicinal chemists capable of rapidly searching for drugs to treat
Parkinson's disease. In a study published online today in Nature Chemical Biology, the
researchers showed that they can rescue yeast cells from toxic levels of a protein
implicated in Parkinson's disease by stimulating the cells to make very small proteins
called cyclic peptides. Two of the cyclic peptides had a protective effect on the yeast
cells and on neurons in an animal model of Parkinson's disease. "This biological
approach to compound development opens up an entirely new direction for drug discovery,
not only for Parkinson's disease, but theoretically for any disease where key aspects of
the pathology can be reproduced in yeast," says Margaret Sutherland, Ph.D., a program
director at NIH's National Institute of Neurological Disorders and Stroke (NINDS). "A
key step for the future will be to identify the cellular pathways that are affected by
these cyclic peptides." The research emerged from the lab of Susan Lindquist, Ph.D.,
a professor of biology at the Massachusetts Institute of Technology (MIT), a member of the
Whitehead Institute for Biomedical Research, and a Howard Hughes Medical Institute
investigator. Dr. Lindquist is also an investigator at the Massachusetts General Hospital
(MGH)/MIT Morris K. Udall Center for Excellence in Parkinson's Research, one of 14 such
centers funded by NINDS to develop treatment breakthroughs for Parkinson's disease. The
study received additional funding from NIH's National Institute of Environmental Health
Sciences, and from the Michael J. Fox Foundation and the American Parkinson's Disease
Association. Parkinson's disease attacks cells in a part of the brain responsible for
motor control and coordination. As those neurons degenerate, the disease leads to
progressive deterioration of motor function including involuntary shaking, slowed
movement, stiffened muscles, and impaired balance. The neurons normally produce a chemical
called dopamine. A synthetic precursor of dopamine called L-DOPA or drugs that mimic
dopamine's action can provide symptomatic relief from Parkinson's disease. Unfortunately,
these drugs lose much of their effectiveness in later stages of the disease, and there is
currently no means to slow the disease's progressive course. In most cases, the cause of
Parkinson's disease is unknown, but there are recent, tantalizing clues. Investigators
have discovered that vulnerable brain cells in patients with Parkinson's disease
accumulate a protein called alpha-synuclein. Moreover, genetic abnormalities in
alpha-synuclein cause a rare familial form of the disease. Dr. Lindquist and her team
previously showed that when yeast cells are engineered to produce large amounts of human
alpha-synuclein, they die. In their new study, Dr. Lindquist and her team tested whether
yeast could make cyclic peptides that would save them from alpha-synuclein's toxicity.
Cyclic peptides are fragments of protein that connect end-to-end to form a circle.
Although cyclic peptides are synthetic, they resemble structures that are found in natural
proteins and protein-based drugs, including pain killers, antibiotics and
immunosuppressants. Cyclic peptides that suppress alpha-synuclein toxicity could be
candidate drugs for Parkinson's disease, or they could help researchers identify new drug
targets for the disease. "Our technique, which capitalizes on a long line of
investigation in my lab, will lead to a whole new way to obtain small molecule tools
useful for improving our understanding of disease mechanisms and for developing new
therapies," says Dr. Lindquist. She notes that her lab and others have modeled many
human diseases in yeast and in other kinds of cells.
New drugs faster from natural
compounds
Researchers have invented computational tools to decode and rapidly determine whether
natural compounds collected in oceans and forests are new—or if these
pharmaceutically promising compounds have already been described and are therefore not
patentable. This University of California, San Diego advance will finally enable
scientists to rapidly characterize ring-shaped nonribosomal peptides (NRPs)—a class
of natural compounds of intense interest due to their potential to yield or inspire new
pharmaceuticals. The study will be published in the July 13 online issue of journal Nature
Methods. "These advances will speed the process by which we discover and describe new
and biologically active molecules from organisms such as marine cyanobacteria, also known
as blue-green algae. This, in turn, will accelerate the timeline for bringing new
experimental therapies into clinical application," said William Gerwick, an author on
the paper and a professor with the UC San Diego Scripps Institution of Oceanography Center
for Marine Biotechnology and Biomedicine and the UCSD Skaggs School of Pharmacy and
Pharmaceutical Sciences.
Swedish researcher finds missing
piece of fossil puzzle
The mode of reproduction seen in modern sharks is nearly 400 million years old. That is
the conclusion drawn by Professor Per Erik Ahlberg, Uppsala University, from his discovery
of a so-called "clasper" in a primitive fossil fish earlier this year. The
research results are published today in Nature. In February this year, a paper published
in Nature by a team of Australian and British researchers showed that placoderms, a group
of ancient fishes that died out more than 350 million years ago, gave birth to live young.
Beautifully preserved fossil embryos in the body cavity of the placoderm Incisoscutum
showed that these fishes, close to the common origin of all jawed vertebrates, had a mode
of reproduction similar to modern sharks. Live birth requires internal fertilisation;
sharks achieve this by using a "clasper", an extension of the pelvic fin that
functions like a penis. The authors looked for a clasper in their placoderm fossils but
couldn't find one, so they were forced to argue that it had been made of soft cartilage
and had not been preserved. Shortly afterwards, Per Erik Ahlberg from Uppsala University
visited one of the Australian researchers and spotted a perfectly preserved bony clasper
in one of their Incisoscutum fossils. "It was lying in plain view but had been
misinterpreted as part of the pelvis and overlooked," he says. Together with the
original authors he is publishing a short paper in this week's Nature that presents this
missing piece of the puzzle and completes the picture of placoderm reproduction from
mating to birth. "It provides a pedigree of nearly 400 million years for the
"advanced" and seemingly specialised reproductive biology of modern
sharks," says Per Ahlberg.
Study may explain why HIV
progresses faster in women than in men with same viral load
One of the continuing mysteries of the HIV/AIDS epidemic is why women usually develop
lower viral levels than men following acute HIV-1 infection but progress faster to AIDS
than men with similar viral loads. Now a research team based at the Ragon Institute of
Massachusetts General Hospital (MGH), MIT and Harvard has found that a receptor molecule
involved in the first-line recognition of HIV-1 responds to the virus differently in
women, leading to subsequent differences in chronic T cell activation, a known predictor
of disease progression. Their paper, which will be published in an upcoming issue of
Nature Medicine, is receiving early online release. "This study may help to account
for reported gender differences in HIV-1 disease progression by demonstrating that women
and men differ in the way their immune systems respond to the virus," says Marcus
Altfeld, MD, PhD, of the Ragon Institute and the MGH Division of Infectious Disease, the
study's senior author. "Focusing on immune activation separately from viral
replication might give us new therapeutic approaches to limiting HIV-1-induced
pathology." It has become apparent in recent years that HIV-1-infected patients with
a high level of immune activation progress to AIDS more rapidly. Why this happens is an
area of intense investigation. To explore whether gender-based differences in immune
activation were responsible for faster disease progression in women, the Ragon Institute
team and their collaborators focused on plasmacytoid dendritic cells (pDCs), among the
first cells of the immune system to respond to HIV-1 and other viral pathogens. Earlier
studies indicated that pDCs recognize HIV-1 using a receptor called Toll-like receptor 7
(TLR7), leading to production of interferon-alpha and other important immune system
molecules. After initial in vitro experiments showed that a higher percentage of pDCs from
uninfected women produced interferon-alpha in response to TLR7 stimulation by HIV-1 than
did cells from uninfected men, the researchers examined whether women's hormone levels had
any effect on pDC activation. Supporting previous evidence that progesterone may modulate
pDC activity, the researchers found that pDCs from postmenopausal women produced levels of
interferon-alpha in response to HIV-1 that were closer to levels observed in men. They
also found that, in premenopausal women, higher progesterone levels correlated with
increased activation of pDCs in response to HIV-1.
Leading pathogen in newborns can
suppress immune cell function
Group B Streptococcus (GBS), a bacterial pathogen that causes sepsis and meningitis in
newborn infants, is able to shut down immune cell function in order to promote its own
survival, according to researchers at the University of California, San Diego School of
Medicine and the Skaggs School of Pharmacy and Pharmaceutical Sciences. Their study,
published online July 13 in the Journal of Experimental Medicine, offers insight into GBS
infection – information that may lead to new medical therapies for invasive
infectious diseases that affect nearly 3,500 newborns in the United States each year. The
UC San Diego researchers describe how GBS fools the immune system into reducing production
of antibiotic molecules. "We have discovered that the bacteria have evolved to use a
trick we call 'molecular mimicry,'" said Victor Nizet, MD, UC San Diego professor of
pediatrics and pharmacy. "Like a wolf in sheep's clothing, GBS can enter our body
without activating the immune cells that are normally programmed to kill foreign
invaders." The findings represent a collaborative effort between the laboratories of
senior authors Nizet and Ajit Varki, MD, distinguished professor of medicine and cellular
and molecular medicine. Varki is also co-director of the UCSD Glycobiology Research and
Training Center, where the investigators have been exploring the interaction of bacterial
pathogens with the innate immune system. Their most recent focus has been on the special
role of Siglecs (short for sialic acid binding Ig-like lectins), members of the
immunoglobulin family of antibodies.
Researchers Testing Virus-Gene
Therapy Combination Against Melanoma
Researchers at the Moores UCSD Cancer Center are injecting a modified herpes virus into
melanoma tumors, hoping to kill the cancer cells while also bolstering the body’s
immune defenses against the disease. Gregory Daniels, MD, PhD, assistant clinical
professor of medicine at the UC San Diego School of Medicine and his co-workers are
comparing the modified virus treatment, called OncoVEX GM-CSF, to general immune system
stimulation with the immune-boosting protein GM-CSF in an international phase III trial
for patients with advanced melanoma. The Moores UCSD Cancer Center is the only site in San
Diego for the clinical trial. Melanoma, the most dangerous kind of skin cancer, takes
about 60,000 lives a year in this country. “Melanoma has always been curable, but
only in a small fraction of patients,” Daniels said. “Local tumor killing with
immune activation may provide an additional tool to increase this number to a larger
population of cancer patients.” According to Daniels, the injected virus appears to
preferentially infect cancer cells, leading to tumor death. The expression of the GM-CSF
protein may also direct an immune attack against both infected and non-infected tumors.
The virus has in essence been genetically reprogrammed to target the cancer cells, while
healthy cells remain relatively untouched. The research team is testing the two-pronged
attack of direct tumor cell killing and immune activation. Their aim is to see if it will
help those patients whose cancer has spread to other areas of the body to live longer
without disease than has been possible with standard therapies.
Early-life experience linked to
chronic diseases later in life
People’s early-life experience sticks with them into adulthood and may render them
more susceptible to many of the chronic diseases of aging, according to a new UBC study. A
team led by UBC researchers Gregory Miller and Michael Kobor performed genome-wide
profiling in 103 healthy adults aged 25-40 years. Those who participated in the study were
either low or high in early-life socioeconomic circumstances related to income, education
and occupation during the first five years of life. But the two groups were similar in
socioeconomic status (SES) at the time the genome assessment was performed and also had
similar lifestyle practices like smoking and drinking habits. Their study, to be published
in this week’s Proceedings of the National Academy of Sciences, shows that among
subjects with low early-life socioeconomic circumstances, there was evidence that genes
involved with inflammation were selectively “switched-on” at some point.
Researchers believe this is because the cells of low-SES individuals were not effectively
responding to a hormone called cortisol that usually controls inflammation.
A special pathway makes bacteria
vulnerable
More and more bacterial stems are developing resistance to previously life-saving
antibiotics. Physicians have been warning that fatality rates from infections could
increase dramatically in the very near future. Researchers at the Technische Universität
München (TUM) have now cast light on a metabolic step that appears in many aggressive
microorganisms like tuberculosis or malaria pathogens and that may provide a promising
target for a new class of antibiotics. The researchers present the results of their work
in the current issue of the chemistry journal "Angewandte Chemie". Antibiotics
hinder the production of essential compounds in microorganisms and can thus hold harmful
pathogens in check. However, ever more bacterial stems are developing multiple antibiotic
resistances, thereby rendering previously life-saving medications ineffective. That is why
researchers around the world are desperately searching for new reaction steps that are
vital to microorganisms but play no relevant role in humans. Professor Michael Groll, Dr.
Jörg Eppinger and Dr. Tobias Gräwert, biochemists at the Technische Universität
München, and their team of researchers have described in detail the structural basis for
just such a reaction step. The cells of virtually all life forms synthesize essential
natural substances belonging to the class of terpenes and steroids from the small isoprene
building blocks dimethylallyl pyrophosphate (DMAPP) and isopentenyl pyrophosphate (IPP).
Mammals and a large number of other organisms generate these essential metabolites via the
so-called mevalonate pathway. But most human pathogens, including Plasmodium falciparum,
have developed an alternate mechanism for producing these important substances. Now, this
special pathway may spell doom for those bacteria. The TUM researchers have unraveled the
structural basis of the terminal step in bacterial isoprene synthesis. The crucial enzyme
has a most unusual structure, similar to a three-leaf clover, and may open a forceful line
of attack for custom-tailored an
U of M Researchers Find Childhood
Cancer Risk Rises with Mother's Age
Research from the Masonic Cancer Center, University of Minnesota indicates that a baby
born to an older mother may have a slightly increased risk for many of the cancers that
occur during childhood. “Our finding shows that although the absolute risk is low,
advancing maternal age may be a factor and explain why, after other factors are adjusted
for, some children get cancer,” said Logan Spector, Ph.D., assistant professor of
pediatrics and cancer epidemiology researcher. Spector and Kimberly Johnson, Ph.D., post
doctoral fellow in pediatric epidemiology, led the research team on this study. The
results are published in the July 2009 issue of the journal Epidemiology. Currently, about
1 in 435 children under the age of 15 in the United States gets cancer. Types of cancers
most often affecting children include leukemia, lymphoma, central nervous system tumor,
neuroblastoma, Wilms’ tumor, bone cancer, and soft tissue sarcoma. For this
population-based case-control study, Spector and Johnson used information from birth
registry records in New York, Washington, Minnesota, Texas, and California. The study
included the records of 17,672 children in those states diagnosed with cancer at ages 0-14
years between 1980 and 2004 and 57,966 children not diagnosed with cancer. “We saw
that the risk of 7 of the 10 most common childhood cancers increased slightly, about 7-10
percent, with every five-year increase in maternal age,” Spector said.
The Biofuel Myth - 44min
Documentary
Biofuel was the buzzword of the millenniums
Green Revolution- an eco-friendly blend of plant oil with regular oil, which could run
your car and produce electricity. Now the global demand for Biofuel is threatening the
lives of the 45 million people who depend on the rainforest for food. A riveting look at
the food vs fuel debate.
Bush Babes - New Zealand
The Long family lives as hermits in South
Westland, New Zealand. They live in a makeshift hut without even the basics of modern life
and have had no contact with the outside world for over 15 years.
Once a young medical student poised for great success, Robert Long decided to relocate his
family to the bush. I wanted to be somewhere where it was all wilderness. Now living
amongst the mountains of New Zealand they thrive from a lifestyle that would terrify most
people. I think they concentrate on what we miss out on, they don't realise how much we
have that they don't have.
Researchers map how staph
infections alter immune system
Infectious disease specialists at UT Southwestern Medical Center have mapped the gene
profiles of children with severe Staphylococcus aureus infections, providing crucial
insight into how the human immune system is programmed to respond to this pathogen and
opening new doors for improved therapeutic interventions. In recent years, research has
focused on understanding precisely what the bacterium S aureus does within the host to
disrupt the immune system. Despite considerable advances, however, it remained unclear how
the host’s immune system responded to the infection and why some people are apt to
get more severe staphylococcal infections than others. By using gene expression profiling,
a process that summarizes how individual genes are being activated or suppressed in
response to the infection, UT Southwestern researchers pinpointed how an individual’s
immune system responds to a S aureus infection at the genetic level.
Study explains potential failure of
oral contraceptives with obese women
Researchers have identified a potential biological mechanism that could explain why oral
contraceptives may be less effective at preventing pregnancy in obese women, as some
epidemiological studies have indicated. Although conventional oral contraceptives appear
to eventually reach the effective blood concentrations needed in the body to prevent
conception in obese women, it appears to take twice as long, leaving a "window of
opportunity" every month where the contraceptive may not be at a high enough level to
prevent a pregnancy. The findings are of particular importance, researchers noted in their
study, because about 30 percent of all adults in the U.S. are obese and the birth control
pill is one of the most popular forms of contraception in the nation. "We don't have
enough data yet to recommend that physicians change their clinical practice for use of
oral contraceptives with patients who are very overweight," said Ganesh Cherala, an
assistant professor in the College of Pharmacy at Oregon State University. "However,
until more studies are done, women may wish to consult with their physicians about this
issue and consider a backup method of contraception at some times of the month." The
study was just published in the journal Contraception, by scientists from OSU, Oregon
Health and Science University, University of Colorado at Denver, Oregon National Primate
Research Center, and the University of Southern California. The research was supported by
the National Institutes of Health. The underlying problem, Cherala said, is that oral
contraceptives, like most drugs, are initially tested in "healthy" people, which
rarely includes people who are more than 130 percent of their ideal body weight.
Ben-Gurion U. researchers identify
how stressed fat tissue malfunctions
Ben-Gurion University of the Negev (BGU) researchers, in a collaboration with colleagues
from the University of Leipzig, Germany, have identified a signaling pathway that is
operational in intra-abdominal fat, the fat depot that is most strongly tied to
obesity-related morbidity. "Fat tissue in obesity is dysfunctional, yet, the
processes that cause fat tissue to malfunction are poorly understood -- specifically, it
is unknown how fat cells 'translate' stresses in obesity into dysfunction," said Dr.
Assaf Rudich, senior lecturer from the Department of Clinical Biochemistry at Ben-Gurion
University. Fat tissue is no longer considered simply a storage place for excess calories,
but in fact is an active tissue that secretes multiple compounds, thereby communicating
with other tissues, including the liver, muscles, pancreas and the brain. Normal
communication is necessary for optimal metabolism and weight regulation. However, in
obesity, fat (adipose) tissue becomes dysfunctional, and mis-communicates with the other
tissues. This places fat tissue at a central junction in mechanisms leading to common
diseases attributed to obesity, like type 2 diabetes and cardiovascular diseases.Fat
tissue dysfunction is believed to be caused by obesity-induced fat tissue stress: Cells
over-grow as they store increasing amounts of fat. This excessive cell growth may cause
decreased oxygen delivery into the tissue; individual cells may die (at least in mouse
models), and fat tissue inflammation ensues. Also, excess nutrients (glucose, fatty acids)
can also result in increased metabolic demands, and this in itself can cause cellular
stress. The BGU and Leipzig teams established a setup for collecting fat tissue samples
from people undergoing abdominal surgery. The team identified a signaling pathway that is
operational in intra-abdominal fat, the fat depot that is most strongly tied to
obesity-related morbidity. The degree of activation of a signaling pathway from these
individuals was compared with those of leaner people, those with obesity predominantly
characterized by accumulation of "peripheral" fat, and those with obesity with
predominant accumulation of fat within the abdominal cavity.
Social reasoning and brain
development are linked in preschoolers -- Queen's study
New research at Queen's University shows that the way preschool children understand false
beliefs can be linked to particular aspects of brain development. This landmark research
may aid in understanding developmental disorders such as autism. One of the most important
ways that preschool children develop socially is by learning how to understand others
people's thoughts and feelings. As they mature, most children discover that people's
thoughts and feelings about the world and the way the world really is may not agree.
"We know that specific areas of the brain are active when adults think about others'
thoughts," says Queen's psychology Professor Mark Sabbagh. "But our findings are
the first to show that these specialized neural circuits are there as early as preschool
years, and that maturational changes in these areas are associated with preschoolers'
abilities to think about their social world in increasingly sophisticated ways."
Researchers compiled EEG results for 29 four-year old children who were engaged in a
series of behavioural tasks, and analyzed the activity levels in different regions of the
brain when assessing whether another person's thoughts and feelings agree with the way the
world really is. Children with more mature patterns of activity in two specific areas
showed more sophisticated understanding of other peoples' false beliefs. By understanding
how the typical social brain develops, researchers can investigate what happens when
social reasoning is impaired, as occurs in autism. "Individuals with autism seem to
have special difficulty understanding false beliefs, which in turn leads to difficulty
with several aspects of social interaction, such as practical aspects of language and
deception," adds Professor Sabbagh. "By studying the specific areas of the brain
identified in our study, researchers may now have starting points for understanding the
neurodevelopmental abnormalities that give underlying autism."
MGH study identifies first
molecular steps to childhood leukemia
A Massachusetts General Hospital (MGH)-based research team has identified how a
chromosomal abnormality known to be associated with acute lymphoblastic leukemia (ALL)
– the most common cancer in children – initiates the disease process. In the
July issue of Cell Stem Cell, they describe how expression of this mutation in
hematopoietic stem cells (HSCs), which usually occurs before birth, leads to the
development of leukemia many years later. "Based on their longevity, it had been
assumed but never shown that HSCs were the cells in which the first steps of leukemia
occur. We now unequivocally demonstrate that HSCs can be involved in the early evolution
of leukemia and that cells expressing an oncogene can continue contributing to blood
formation while serving as a hard-to-detect reservoir of malignancy-prone cells,"
says Hanno Hock, MD, PhD, of the MGH Cancer Center and Center for Regenerative Medicine,
corresponding author of the Cell Stem Cell article. "We hope that better
understanding the latency period of childhood leukemia will help us interfere with the
disease earlier and in a more targeted, less toxic manner." Acute lymphoblastic
leukemia (ALL) represents 23 percent of all cancer diagnoses in children under 15.
Although treatment of childhood ALL has been a major success story, with 85 percent of
patients surviving five years or more, it involves two to three years of complex
chemotherapy. Studies have identified leukemia-associated genetic and molecular
abnormalities that can precede development of symptoms by several years and also pointed
to a chromosomal translocation called TEL-AML1 as the first step toward ALL. But how and
in which cells this process begins was not clear. Previous examinations of the role of the
TEL-AML1 allele in initiating ALL, conducted using less refined systems, had inconsistent
results. In the current study, the research team developed a mouse model in which they
could induce the expression of TEL-AML1 at various stages of blood cell development using
the same chromosomal regulatory elements active in leukemic cells. They found that, when
the mutation is expressed in more differentiated progenitor cells, those cells do not
survive long enough to acquire subsequent mutations required for malignant transformation.
But expression of TEL-AML1 in HSCs, the only blood-forming cells that continually renew
themselves, leads to a persistent overpopulation of altered HSCs that are particularly
sensitive to secondary, transformational mutations.
Surprising new insights into the
repair strategies of DNA
A microscopic single-celled organism, adapted to survive in some of the harshest
environments on earth, could help scientists gain a better understanding of how cancer
cells behave. Experts at The University of Nottingham were astonished to discover that the
archaeon Haloferax volcanii was better at repairing DNA damage if enzymes, that are widely
considered to be critically important in coordinating the repair of DNA, were mutated. Dr
Thorsten Allers, from the Institute of Genetics, said: “These results surprised us.
It is the first time, as far as we know, that anybody has found such resistance to DNA
damage in mutant cells. Normally, cells that are missing enzymes for DNA repair become
more sensitive to DNA damage.”
Vitamin D, curcumin may help clear
amyloid plaques found in Alzheimer's disease
UCLA scientists and colleagues from UC Riverside and the Human BioMolecular Research
Institute have found that a form of vitamin D, together with a chemical found in turmeric
spice called curcumin, may help stimulate the immune system to clear the brain of amyloid
beta, which forms the plaques considered the hallmark of Alzheimer's disease .The early
research findings, which appear in the July issue of the Journal of Alzheimer's Disease,
may lead to new approaches in preventing and treating Alzheimer's by utilizing the
property of vitamin D3 — a form of vitamin D — both alone and together with
natural or synthetic curcumin to boost the immune system in protecting the brain against
amyloid beta. Vitamin D3 is an essential nutrient for bone and immune system health; its
main source is sunshine, and it is synthesized through the skin. Deficiencies may occur
during winter months or in those who spend a lot of time indoors, such as Alzheimer's
patients. "We hope that vitamin D3 and curcumin, both naturally occurring nutrients,
may offer new preventive and treatment possibilities for Alzheimer's disease," said
Dr. Milan Fiala, study author and a researcher at the David Geffen School of Medicine at
UCLA and the Veterans Affairs Greater Los Angeles Healthcare System. Using blood samples
from nine Alzheimer's patients, one patient with mild cognitive impairment and three
healthy control subjects, scientists isolated monocyte cells, which transform into
macrophages that act as the immune system's clean-up crew, traveling through the brain and
body and gobbling up waste products, including amyloid beta. Researchers incubated the
macrophages with amyloid beta, vitamin D3 and natural or synthetic curcumin. The synthetic
curcuminoid compounds were developed in the laboratory of John Cashman at the Human
BioMolecular Research Institute, (http://www.hbri.org/), a nonprofit institute dedicated
to research on diseases of the human brain.Researchers found that naturally occurring
curcumin was not readily absorbed, that it tended to break down quickly before it could be
utilized and that its potency level was low, making it less effective than the new
synthetic curcuminoids. "We think some of the novel synthetic compounds will get
around the shortcomings of curcumin and improve the therapeutic efficacy," Cashman
said. The team discovered that curcuminoids enhanced the surface binding of amyloid beta
to macrophages and that vitamin D strongly stimulated the uptake and absorption of amyloid
beta in macrophages in a majority of patients.
Study reveals major genetic
differences between blood and tissue cells
Research by a group of Montreal scientists calls into question one of the most basic
assumptions of human genetics: that when it comes to DNA, every cell in the body is
essentially identical to every other cell. Their results appear in the July issue of the
journal Human Mutation.This discovery may undercut the rationale behind numerous
large-scale genetic studies conducted over the last 15 years, studies which were supposed
to isolate the causes of scores of human diseases. Except for cancer, samples of diseased
tissueare difficult or even impossible to take from living patients. Thus, the vast
majority of genetic samples used in large-scale studies come in the form of blood.
However, if it turns out that blood and tissue cells do not match genetically, these
ambitious and expensive genome-wide association studies may prove to have been essentially
flawed from the outset. This discovery sprang from an investigaton into the underlying
genetic causes of abdominal aortic aneurysms (AAA) led by Dr. Morris Schweitzer, Dr. Bruce
Gottlieb, Dr. Lorraine Chalifour and colleagues at McGill University and the affiliated
Lady Davis Institute for Medical Research at Montreal's Jewish General Hospital. The
researchers focused on BAK, a gene that controls cell death. What they found surprised
them. AAA is one of the rare vascular diseases where tissue samples are removed as part of
patient therapy. When they compared them, the researchers discovered major differences
between BAK genes in blood cells and tissue cells coming from the same individuals, with
the suspected disease "trigger" residing only in the tissue. Moreover, the same
differences were later evident in samples derived from healthy individuals. "In
multi-factorial diseases other than cancer, usually we can only look at the blood,"
explained Gottlieb, a geneticist with McGill's Centre for Translational Research in
Cancer. "Traditionally when we have looked for genetic risk factors for, say, heart
disease, we have assumed that the blood will tell us what's happening in the tissue. It
now seems this is simply not the case." "From a genetic perspective, therapeutic
implications aside, the observation that not all cells are the same is extremely
important. That's the bottom line," he added. "Genome-wide association studies
were introduced with enormous hype several years ago, and people expected tremendous
breakthroughs. They were going to draw blood samples from thousands or hundreds of
thousands of individuals, and find the genes responsible for disease. "Unfortunately,
the reality of these studies has been very disappointing, and our discovery certainly
could explain at least one of the reasons why."
New evidence that popular dietary
supplement may help prevent, treat cataracts
Researchers are reporting evidence from tissue culture experiments that the popular
dietary supplement carnosine may help to prevent and treat cataracts, a clouding of the
lens of the eye that is a leading cause of vision loss worldwide. The study is scheduled
for the July 28 edition of ACS' Biochemistry, a weekly journal. In the new study, Enrico
Rizzarelli and colleagues note that the only effective treatment for cataracts is surgical
replacement of the lens, the clear disc-like structure inside the eye that focuses light
on the nerve tissue in the back of the eye. Cataracts develop when the main structural
protein in the lens, alpha-crystallin, forms abnormal clumps. The clumps make the lens
cloudy and impair vision. Previous studies hinted that carnosine may help block the
formation of these clumps. The scientists exposed tissue cultures of healthy rat lenses to
either guanidine — a substance known to form cataracts — or a combination of
guanidine and carnosine. The guanidine lenses became completely cloudy, while the
guanidine/carnosine lenses developed 50 to 60 percent less cloudiness. Carnosine also
restored most of the clarity to clouded lenses. The results demonstrate the potential of
using carnosine for preventing and treating cataracts, the scientists say.
Fighting drug-resistant flu viruses
Amid reports that swine flu viruses are developing the ability to shrug off existing
antiviral drugs, scientists in Japan are reporting a first-of-its kind discovery that
could foster a new genre of antivirals that sidestep resistance problems, according to an
article scheduled for the July 23 issue of the ACS' Journal of the Medicinal Chemistry, a
bi-weekly publication. Toshinori Sato and colleagues note in the new study that current
antiviral drugs, including Tamiflu and Relenza, fight influenza by blocking key proteins
that viruses need to reproduce. As the viruses reproduce, however, they can mutate into
drug-resistant strains. The researchers describe discovery of a new way to prevent flu
viruses from infecting cells in the first place. They identified potential drugs that can
block the first step in the infection process, and demonstrated that the substances work
in cell cultures. "These results may lead to a new approach in the design of
antiviral drugs," they state, noting that it could be used to develop new drugs for a
variety of other medical problems.
A Chemical Reaction- Trailer
A Chemical Reaction, is a documentary movie
scheduled for release in 2009 that tells the story of one of the most powerful and
effective community initiatives in the history of North America.
New genetic study of Asperger
syndrome, autistic traits and empathy
Scientists from the University of Cambridge have identified 27 genes that are associated
with either Asperger Syndrome (AS) and/or autistic traits and/or empathy. The research
will be published tomorrow in the journal Autism Research. This is the first candidate
gene study of its kind. The research was led by Dr Bhismadev Chakrabarti and Professor
Simon Baron-Cohen from the Autism Research Centre in Cambridge. 68 genes were chosen
either because they were known to play a role in neural growth, social behaviour, or sex
steroid hormones (e.g. testosterone and estrogen). The latter group of genes was included
because AS occurs far more often in males than females, and because previous research from
the Cambridge team has shown that foetal testosterone levels are associated with autistic
traits and empathy in typically developing children. The team carried out 2 experiments.
First they looked at these genes in 349 adults in the general population, all of whom had
filled in the Autism Spectrum Quotient (AQ) as a measure of autistic traits, and the
Empathy Quotient (EQ) as a measure of empathy. Secondly, they looked at 174 adults with a
formal diagnosis of AS, and compared them to controls. The research found that single
nucleotide polymorphisms (SNPs) in 27 out of the 68 genes were nominally associated with
either AS and/or with autistic traits/empathy. 10 of these genes (such as CYP11B1) were
involved with sex steroid function, providing support for the role of this class of genes
in autism and autistic traits. 8 of these genes (such as NTRK1) were involved in neural
growth, providing further support to the idea that autism and autistic traits could result
from aberrant patterns of connectivity in the developing brain. The other 9 genes (such as
OXTR) were involved in social behaviour, shedding light on the biology of social and
emotional sensitivity. Dr Chakrabarti commented: "These 27 genes represent
preliminary leads for understanding the genetic bases of AS and related traits, such as
empathy, in the general population. All of these are good candidates for independent
replication studies in both low and high functioning autism samples. 5 of the genes we
found have been previously reported in autism, but the other 22 have never before been
reported in association with AS, autistic traits or empathy. We now need to test models of
how these genes interact and construct 'risk' models for the development of AS."
DACH1 a key protein for tumor
suppression in ER+ breast cancer
Researchers from the Kimmel Cancer Center at Jefferson have identified a protein
relationship that may be an ideal treatment target for ER+ breast cancer. The study was
reported in the July 15 issue of Cancer Research. DACH1, a cell fate determination factor
protein, prevents cancer cell proliferation by repressing the function of estrogen
receptors in breast cancer, the researchers found. However, they also found that as the
presence of DACH1 decreases in breast cancer, the presence of estrogen receptors
increases, and vice versa. Approximately 70% of breast cancers are ER+. Treatment for ER+
breast cancer usually consists of hormone therapy, which includes lowering the natural
estrogen levels in the body or using synthetic drugs like tamoxifen, which compete with
natural estrogen. However, this treatment only works for a few years. "Eventually,
cancer cells will circumvent the estrogen-dependent growth and find a different pathway
through which they will proliferate," said Vladimir Popov, a doctoral student in
Biochemistry and Molecular Biology at Jefferson College of Graduate Studies of Thomas
Jefferson University and the study's first author. "Our lab has shown that there is a
correlation between DACH1 and estrogen receptors. DACH1 is a naturally occurring repressor
of estrogen receptor function in normal breast tissue, which makes it a promising
therapeutic target for patients with ER+ breast cancer." DACH1 is expressed in normal
breast tissue. As breast cancer develops and becomes more invasive, the expression of
DACH1 decreases. In a previous study of more than 2,000 breast cancer patients, Jefferson
researchers found that a lack of DACH1 expression was associated with a poor prognosis.
Patients who did express DACH1 lived an average of 40 months longer. "Many more
studies need to be done, but there is strong evidence that DACH1 is a promising marker of
survival and therapeutic target in patients with breast cancer," said the study's
senior researcher Richard Pestell, M.D., Ph.D, who is director of the Kimmel Cancer Center
and chair of the Cancer Biology department at Jefferson.
Circulating blood cells are
important predictors of cancer spread in children
Endothelial progenitor cells may play a role in the start and progression of metastatic
disease in children with cancer, according to study results published in Clinical Cancer
Research, a journal of the American Association for Cancer Research. "This is the
first study to measure circulating endothelial cells and endothelial progenitor cells in
children with cancer, which can provide insight as to the biology of their tumor
vessels," said researcher Françoise Farace, Ph.D., director of the department of
biology of circulating cells in the translational research laboratory, Institut Gustave
Roussy, France. "Not only were these cells found in higher levels in patients
compared to healthy volunteers, but endothelial progenitor cells were found in strikingly
higher amounts in patients with metastatic disease," Farace said. Circulating
endothelial cells are rare cells that shed from the lining of blood vessels after vascular
damage. Both circulating endothelial cells and their precursors, endothelial progenitor
cells, have been described in previous studies, but mainly in the context of
cardiovascular disease. Farace and colleagues measured circulating mature endothelial
cells and bone marrow-derived endothelial progenitor cells in pediatric patients with
solid tumors. They collected blood from 23 patients with localized disease, 22 patients
with metastatic disease and 20 healthy participants and measured subsets of circulating
cells. While the researchers were not surprised to detect circulating endothelial cells
and endothelial progenitor cells in pediatric patients, they were surprised to find these
cell levels were significantly higher in patients with metastatic disease compared to
levels found in healthy participants. "This implies that these endothelial cells most
likely play a role in the development of cancer in children," Farace said. "We
also observed a large range of cell levels in patients with various tumor types. In some
cases, very high levels were observed, which means that their role may be very
important."
Phase 3 Alzheimer's drug increases
toxic beta amyloid in the brain
New insights into how a Phase III Alzheimer's drug might work were among the advances in
potential therapies targeting two abnormal brain proteins – beta amyloid and
phosphorylated tau – that were reported today at the Alzheimer's Association 2009
International Conference on Alzheimer's Disease (ICAD 2009) in Vienna. Scientists also
reported on how clinicians view and treat mild cognitive impairment (MCI), a research
category used to define the state between normal aging and Alzheimer's, that is now being
used widely in clinical practice. "There are now more than 5 million people living
with Alzheimer's disease in the United States. The cost of caring for people who now have
Alzheimer's, and those who will get it in the next few years, will bankrupt the healthcare
system and devastate Medicare and Medicaid," said Ralph Nixon, PhD, MD, vice chair of
the Alzheimer's Association Medical & Scientific Advisory Council. "But, as these
studies and many hundreds more reported at ICAD 2009 show, there is hope. There are
currently dozens of drugs in Phase II and III clinical trials for Alzheimer's. This,
combined with advancements in diagnostic tools, has the potential to change the landscape
of Alzheimer's in our lifetime. How fast we get there depends completely on the investment
in research. We need more government and private dollars for Alzheimer's research now to
capitalize on the progress we've made in the last decade," Nixon added. Surprisingly,
Dimebolin Increases Brain Beta Amyloid in Alzheimer's Mouse Models
Stop the pretence - The EU opens on
Bastille day
Study sheds light on social brain
development
The capacity to figure out what others are thinking and what they mean is an ability
unique to people that's central to our lives. A new study on the neural mechanisms that
govern these abilities sheds light on the relation between how people and groups interact,
on the one hand, and how the brain develops and functions, on the other. The study, in the
July/August 2009 issue of the journal Child Development, was conducted by researchers at
Queen's University at Kingston in Ontario, Canada. In the preschool years, children
develop social skills by learning how to understand others' thoughts and feelings, or
their theory of mind. In most children, theory of mind changes over time so they come to
understand that others' thoughts are representations of the world that may or may not
match the way the world actually is. In their study of EEGs of 29 4-year-olds, the
researchers found that these changes are related to the functional development of two
parts of the brain—the dorsal medial prefrontal cortex and the temporal-parietal
juncture—that govern similar understanding in adults. "For a while now, we have
known that specific brain areas are used when adults think about others' thoughts,"
according to Mark A. Sabbagh, associate professor of psychology at Queen's University at
Kingston and the study's lead author. "Our findings are the first to show that these
specialized neural circuits may be there as early as the preschool years, and that
maturational changes in these areas are associated with preschoolers' abilities to think
about their social world in increasingly sophisticated ways.
Fetal short-term memory found in
30-week-old fetuses
Memory probably begins during the prenatal period, but little is known about the exact
timing or for how long memory lasts. Now in a new study from the Netherlands, scientists
have found fetal short-term memory in fetuses at 30 weeks. The study provides insights
into fetal development and may help address and prevent abnormalities. Published in the
July/August 2009 issue of the journal Child Development, it was conducted by researchers
at Maastricht University Medical Centre and the University Medical Centre St. Radboud. The
scientists studied about 100 healthy pregnant Dutch women and their fetuses, measuring
changes in how the fetus responds to repeated stimulation. After receiving a number of
stimuli, the fetus no longer responds to the stimulus as observed by ultrasonography and
the stimulus is then accepted as "safe." This change in response is called
"habituation." In a second session, the fetus "remembers" the stimulus
and the number of stimuli needed for the fetus to habituate is then much smaller. Based on
their research, the scientists found the presence of fetal short-term memory of 10 minutes
at 30 weeks. They determined this because a significantly lower number of stimuli was
needed to reach habituation in a second session, which was performed 10 minutes after the
first session. They also found that 34-week-old fetuses can store information and retrieve
it four weeks later. Fetuses were tested at 30, 32, 34, and 36 weeks, and again at 38
weeks. The 34- and 36-week-old fetuses habituated much faster than the 38-week-old fetuses
that had not been tested before. This implies that these fetuses have a memory of at least
4 weeks—the interval between the test at 34 weeks and that at 38 weeks. "A
better understanding of the normal development of the fetal central nervous system will
lead to more insight into abnormalities, allowing prevention or extra care in the first
years of life and, as a consequence, fewer problems in later life," according to the
study's authors.
Bird population declines in
northern Europe are explained by thiamine (vitamin B1) deficiency
Wild birds of several species are dying in large numbers from a paralytic disease with
hitherto unknown cause in the Baltic Sea area. A research team at Stockholm University,
Sweden, led by Associate Professor Lennart Balk, has demonstrated strong relationships
between this disease, breeding failure, and advanced thiamine (vitamin B1) deficiency in
eggs, young, and adults. The results are presented in the article "Wild birds of
declining European species are dying from a thiamine deficiency syndrome", published
in the on-line Early Edition of the well-reputed journal Proceedings of the National
Academy of Sciences, USA (PNAS). Thiamine is an essential nutrient for birds and other
vertebrates. In the living cell, its phosphorylated form acts as a cofactor for several
life sustaining enzymes, which are non-functional if the cofactor is missing. Thiamine is
also necessary for the proper functioning of the nerves. Thiamine deficiency was
demonstrated in the egg, liver, and brain as reduced thiamine concentrations, and in the
liver and brain as reduced activities of the thiamine-dependent enzymes. In the liver and
brain, there were also elevated proportions of these enzymes without the thiamine
cofactor. Moreover, paralysed individuals were successfully remedied by thiamine
treatment. The excess mortality and breeding failure are part of a thiamine deficiency
syndrome, which most probably has contributed significantly to declines in many bird
populations during the last decades.
Hospital workers smoking –
only the most addicted flout the rules
A survey of staff at Addenbrooke’s hospital has shown that those who break the
smoke-free policy are generally more addicted than those who respect it. Researchers
writing in the open access journal BMC Public Health also investigated staff’s
attitude to the smoke-free policy and found that smokers were less likely to believe that
the policy would protect people from second hand smoke. With funding from the
Addenbrooke’s Charitable Trust, Tom Parks was one of a team of four medical students
from the University of Cambridge School of Clinical Medicine (UK), based at
Addenbrooke’s, who carried out the survey. He said, “We found that those who
smoke in contravention to the smoke-free policy do so neither for pleasure nor to avoid
feeling low; instead it is a resistant habit, which has little or no influence on the
smoker’s mood, and is determined in part by chemical dependence”. All 6,981
members of staff at the hospital were given the opportunity to take part in the anonymous
survey, and 704 completed and returned the questionnaires. Among the 101 smokers, 69 were
compliant with the hospital's smoke-free policy while 32 were non-compliant. Gender, age
and ethnicity were similar between compliant and non-compliant smokers. Contract ancillary
workers were less likely to comply, while clerical and managerial staff were more likely
to comply.
Relation between local food
environments and obesity among adults
In summary, the current study was the first to find that relative availability of
different types of food retailers around peoples' homes was associated with obesity in a
Canadian context. Similarly, it was among the first to document such associations outside
of the United States. As our findings held regardless of neighbourhood- and
individual-level SES, a plausible policy option for decreasing the prevalence of obesity
among adults is improving the retail food environment, possibly through zoning by-laws. A
recent systematic review of urban environment and healthy weights [48] revealed a variety
of policy options have been proposed in Canada, but not systematically implemented or
evaluated. Thus, future research on effectiveness of interventions to improve health and
weight outcomes at the urban environment level is warranted.
The role of genetic factors in
adult ADHD
Attention deficit/hyperactivity disorder, or ADHD, is one of the most common
neuropsychiatric disorders of childhood. Worldwide, 3–12% of children are affected
with the disorder, whose symptoms include age-inappropriate hyperactive and impulsive
behaviour and/or a reduced ability to focus attention. ADHD has classically been viewed as
a disorder of children, but the majority of patients carries ADHD symptoms, or even the
full ADHD-diagnosis, into adulthood. This leads to social and professional problems and is
associated with considerable costs. Converging evidence suggests that ADHD aetiology has a
robust genetic component. The heritability of the adult form of ADHD appears even higher
than that of children. With the adult form of ADHD being the most severe one, focusing on
the genetics of ADHD in adults can be expected to guide future research in this
challenging field. For that reason, a group of researchers focusing on the genetics of
adult ADHD decided to pool their efforts in the International Multicentre persistent ADHD
CollaboraTion (IMpACT), investigating the largest clinical ADHD sample worldwide. Dr.
Barbara Franke, Ph.D., who is coordinating this promising research project, will present
the latest findings in the identification of risk genes for ADHD. She will explain how the
findings of IMpACT may help to define targets for the development of new and more
effective treatments for ADHD, and also contribute to early disease prevention.
Study finds survival rates from
gastrointestinal tumors improving among African-Americans
New research published in the July issue of the Journal of the American College of
Surgeons reveals that African Americans with gastrointestinal stromal tumors (GIST), a
rare cancer that begins in the wall of the gastrointestinal tract, now have survival rates
equivalent to those of Caucasians. Prior to 2000, African Americans were more likely to
develop GIST and less likely to undergo surgical treatment for this type of cancer. Racial
disparities in survival rates have been demonstrated for a number of cancers, typically
due to unequal access to care. Through the National Institutes of Health and Healthy
People 2010, a national health promotion and disease prevention initiative, the federal
government has set forth goals to explore, account for and minimize these disparities.
"Over the last decade, racial gaps in the treatment of GIST appeared to have
closed," said Michael Cheung, MD, DeWitt Daughtry Family Department of Surgery,
University of Miami, Miller School of Medicine. "Both perioperative and long-term
survival have improved among African Americans."
New technique could sustain cancer
patients' fertility
Researchers funded by the National Institutes of Health have completed a critical first
step in the eventual development of a technique to retain fertility in women with cancer
who require treatments that might otherwise make them unable to have children. The
researchers have developed a method to advance undeveloped human eggs to near maturity, in
laboratory cultures maintained outside the body. The technique focuses on the follicle, a
tiny sac within the ovary that contains the immature egg. The researchers were able to
grow human follicles in the laboratory for 30 days, until the eggs they contained were
nearly mature. The research seeks to provide women who require a fertility-ending
treatment with options for reproduction after their treatment is complete. Men facing such
treatments can freeze their sperm for use at a later date. Female cancer patients have
fewer options. Unlike sperm, eggs rarely survive freezing and thawing. The accomplishment
represents the successful completion of the first of three steps needed to preserve a
woman's fertility after radiation treatments or chemotherapy. For the next step,
researchers will need to induce the egg's final division, so that it contains only half
the genetic material of its precursors. Finally, the researchers will have to demonstrate
that they can freeze and thaw human follicles before growing them in culture. "The
new technique could provide an option for women and girls who have cancer and are not yet
ready to start families," said Duane Alexander, M.D., director of NIH's Eunice
Kennedy Shriver National Institute of Child Health and Human Development (NICHD), which
funded the research as part of the NIH Roadmap Interdisciplinary Research Consortium
program. "An additional benefit is that it will allow researchers to more closely
follow the process by which immature eggs grow and mature. In turn, these observations may
lead to new advances for treating other forms of infertility." The best option
currently for a female cancer patient to preserve fertility is to collect eggs, fertilize
them with sperm, and freeze the resulting embryos. But that technique may not be
acceptable to all female cancer patients. Researchers have already identified experimental
methods to freeze entire ovaries or strips of ovarian tissue and implant them in a woman's
body when she is ready to have children. This is a good option for some patients, but it
is possible that some cancer cells may hitch hike on the ovarian tissue and result in a
new cancer after treatment is completed.
Obesity contributes to rapid
cartilage loss
Obesity, among other factors, is strongly associated with an increased risk of rapid
cartilage loss, according to a study published in the August issue of Radiology. "We
have isolated demographic and MRI-based risk factors for progressive cartilage loss,"
said the study's lead author, Frank W. Roemer, M.D., adjunct associate professor at Boston
University and co-director of the Quantitative Imaging Center at the Department of
Radiology at Boston University School of Medicine. "Increased baseline body mass
index (BMI) was the only non-MRI-based predictor identified." Tibio-femoral cartilage
is a flexible connective tissue that covers and protects the bones of the knee. Cartilage
damage can occur due to excessive wear and tear, injury, misalignment of the joint or
other factors, including osteoarthritis. Osteoarthritis is the most common form of
arthritis, affecting 27 million Americans, according to the National Institute of
Arthritis and Musculoskeletal and Skin Diseases. In osteoarthritis, the cartilage breaks
down and, in severe cases, can completely wear away, leaving the joint without a cushion.
The bones rub together, causing further damage, significant pain and loss of mobility. The
best way to prevent or slow cartilage loss and subsequent disability is to identify risk
factors early. "Osteoarthritis is a slowly progressive disorder, but a minority of
patients with hardly any osteoarthritis at first diagnosis exhibit fast disease
progression," Dr. Roemer said. "So we set out to identify baseline risk factors
that might predict rapid cartilage loss in patients with early knee osteoarthritis or at
high risk for the disease."
Study by NTU professors provides
important insight into apoptosis or programmed cell death
A study by Nanyang Technological University (NTU)'s Assistant Professor Li Hoi Yeung,
Assistant Professor Koh Cheng Gee and their team have made an important contribution to
the understanding of the process that cells go through when they die. This process known
as 'apoptosis' or programmed cell death, is a normal process in the human body which
removes perhaps a million cells a second. According to Professor Li, they discovered that
during apoptosis, the cell's rescue mechanism is inhibited when certain proteins (i.e.
'anti-factors' that are necessary to keep a cell alive) are no longer able to enter the
cell's nucleus, thus stopping the cell's ability to initiate its self-repair process. In
addition, they also discovered that the protein RanGTP, which is involved in the
transportation of certain proteins into and out of the cell's nucleus, is reduced greatly
during the early stages of apoptosis. Under normal circumstances, there is a high
distribution of RanGTP in the nucleus and a low concentration of RanGTP in the cytoplasm
(the body enveloping the cell's nucleus). It is this gradient of RanGTP that exist across
the nuclear-cytoplasmic boundaries that serves as a track and directs the transport of
proteins and other molecules into and out of the nucleus. Hence, when the concentration of
RanGTP is reduced in the nucleus, the RanGTP gradient collapses and the nuclear transport
machinery subsequently shuts down.Too little or too much apoptosis plays a role in a great
many diseases. When programmed cell death does not work right, cells that should be
eliminated may linger around and become immortal - for example, in cancer and leukemia.
When apoptosis works overly well, it kills too many cells and inflicts grave tissue
damage. This is the case in strokes and neurodegenerative disorders such as Alzheimer,
Huntington and Parkinson diseases.
NOAA bans commercial harvesting of
krill
The National Oceanic and Atmospheric Administration (NOAA) today published a final rule in
the Federal Register prohibiting the harvesting of krill in the Exclusive Economic Zone
(EEZ) off the coasts of California, Oregon, and Washington. The rule goes into effect on
August 12, 2009. Krill are a small shrimp-like crustacean and a key source of nutrition in
the marine food web. "Krill are the foundation for a healthy marine ecosystem,"
said Mark Helvey, NOAA's Fisheries Service Southwest Assistant Regional Administrator for
Sustainable Fisheries. "Protecting this vital food resource will help protect and
maintain marine resources and put federal regulations in line with West-Coast
states." While the States of California, Oregon and Washington currently have
regulations prohibiting the harvesting of krill within three miles of their coastlines,
there was no similar federal restriction within the three to 200-mile confines of the EEZ.
The krill prohibition was adopted as Amendment 12 to the Coastal Pelagic Species Fishery
Management Plan (FMP), which was developed by the Pacific Fishery Management Council
(PFMC) under the Magnuson-Stevens Fishery Conservation and Management Act. The krill
harvest prohibition was originally proposed to the PFMC and NOAA Fisheries Service by
NOAA's Office of National Marine Sanctuaries. Today's rule implements Amendment 12 to the
FMP and is intended to preserve key nutritional relationships in the California Current
ecosystem, which includes five National Marine Sanctuaries.
Researchers Identify Specific
Pesticide Linked To Parkinson’s Disease
A team of researchers have identified elevated serum levels of the pesticide
?-hexachlorocyclohexane (?-HCH) in patients with Parkinson’s disease, indicating that
exposure to a specific pesticide may contribute to the development of the disease. The
study, published today in Archives of Neurology, is a collaboration of research teams led
by Jason R. Richardson, PhD, assistant professor of environmental and occupational
medicine at UMDNJ-Robert Wood Johnson Medical School and resident member of the
Environmental and Occupational Health Sciences Institute, a joint institute of Robert Wood
Johnson Medical School and Rutgers University, and Dwight C. German, PhD, professor of
psychiatry at the University of Texas Southwestern Medical Center, Dallas, TX. ?-HCH is an
insecticide that was used widely in the United States from the 1950s through the 1970s in
agriculture. ?-HCH also is found as a contaminant of the insecticide lindane, which was
used in treatments for fleas and ticks in pets and in treatments for lice and mange in
humans until recently. Although its use was banned in the 1970’s, ?-HCH is still
found as a persistent environmental contaminant in water and soil. “Previous studies
established the link between pesticides and neurodegenerative diseases, but most had not
identified specific pesticides that may be associated with an increased risk of developing
Parkinson’s,” said Dr. Richardson. “This discovery provides a foundation
upon which to research the precise implications of ?-HCH’s role in the cause of the
disease and how ?-HCH’s levels may be affected by other possible factors such as
genetic disposition and lifestyle choices.” In the study, the researchers measured
the levels of 16 pesticides in blood samples from patients with Parkinson’s or
Alzheimer’s disease and a control group with no neurological disease. The researchers
detected ?-HCH in 76 percent of the patients with Parkinson’s, 40 percent of the
control patients and 30 percent of the patients with Alzheimer’s. In addition to
being more frequently detected in Parkinson’s patients, the amount of ?-HCH in the
serum of Parkinson’s patients was much higher than in the controls. The study
indicated that there was no significant difference in the levels of the other 15
pesticides measured among the study participants. According to the researchers, detection
of ?-HCH in the serum of the control group, although at a lower level, suggests that other
factors may interact with ?-HCH to increase the risk of Parkinson’s. Moving forward,
the researchers plan to expand the study population and work to understand if there is a
correlation between ?-HCH serum levels and other possible risk factors including, but not
limited to, genetics, diet or gender.
Mayo Clinic study using structural
MRI may help accurately diagnose dementia patients
- A new Mayo Clinic study may help physicians differentially diagnose three common
neurodegenerative disorders in the future. The study will be presented at the Alzheimer's
Association International Conference on Alzheimer's Disease on July 11 in Vienna. In this
study, Mayo Clinic researchers developed a framework for MRI-based differential diagnosis
of three common neurodegenerative disorders: Alzheimer's disease, frontotemporal lobar
degeneration, and Lewy body disease using Structural MRI. Currently, examination of the
brain at autopsy is the only way to confirm with certainty that a patient had a specific
form of dementia. The framework, which is called "STructural Abnormality iNDex"
or STAND-Map, shows promise in accurately diagnosing dementia patients while they are
alive. The rationale is that if each neurodegenerative disorder can be associated with a
unique pattern of atrophy specific on MRI, then it may be possible to differentially
diagnose new patients. The study looked at 90 patients from the Mayo Clinic database who
were confirmed to have only a single dementia pathology and also underwent an MRI at the
time of clinical diagnosis of dementia. Using the STAND-Map framework, researchers
predicted an accurate pathological diagnosis 75 to 80 percent of the time. "The
STAND-Map framework might have great potential in early diagnosis of dementia
patients," says Prashanthi Vemuri, Ph.D., a senior research fellow at the Mayo Clinic
aging and dementia imaging research lab and lead author of the study. "The next step
would be to test the framework on a larger population to see if we can replicate these
results and improve the accuracy level we achieved in this proof of concept study. In
turn, this may lead to better treatment options for dementia patients."
Easy strength training exercise may
help treat tennis elbow, study shows
People with pain in the elbow or forearm from playing sports or just from common everyday
activities, might be able to use a simple bar and strengthening exercise to alleviate
pain, say researchers who are presenting their study results at the American Orthopaedic
Society for Sports Medicine's Annual Meeting in Keystone, Colorado, July 9th-12th. Tennis
elbow or lateral epicondylitis is a common condition effecting nearly three percent of the
general population, not just those who play tennis. "Our study illustrated that a
novel exercise, using an inexpensive rubber bar, may provide a practical and effective
means of adding isolated wrist strengthening exercises to a treatment plan," said
lead author Timothy F. Tyler, PT, ATC, Clinical Research Associate, of the Nicholas
Institute of Sports Medicine and Athletic Trauma in New York City. The study randomized 21
patients with tennis elbow into two groups. Both received the wrist extensor stretching,
ultrasound, cross-friction massage, heat and ice for treatment. The eccentric training
group performed isolated eccentric wrist extensor strengthening using the rubber bar
(Flexbar, Akron OH) while the standard treatment group performed isotonic wrist
strengthening exercises. Three sets of 15 repetitions were performed daily as part of a
home program with intensity increased progressively during the treatment period. A variety
of pain and movement scales were utilized to determine progress. Patients using the rubber
bar had vastly better results on all scales, especially related to strength. In fact,
given the consistently poor outcomes for patients in the standard treatment group, it was
deemed appropriate to terminate the randomization with 21 of the intended 30 patients
having already completed the study. "Compared to other treatments for tennis elbow
such as cortisone injections or topical nitric oxide which require direct medical
supervision and often side effects, this treatment is not only cost effective but dosage
is not limited by the patient having to come to a clinic," said Tyler.
Telomeres resemble DNA fragile
sites
Telomeres, the repetitive sequences of DNA at the ends of linear chromosomes, have an
important function: They protect vulnerable chromosome ends from molecular attack.
Researchers at Rockefeller University now show that telomeres have their own weakness.
They resemble unstable parts of the genome called fragile sites where DNA replication can
stall and go awry. But what keeps our fragile telomeres from falling apart is a protein
that ensures the smooth progression of DNA replication to the end of a chromosome.The
research, led by Titia de Lange, head of the Laboratory of Cell Biology and Genetics, and
first author Agnel Sfeir, a postdoctoral associate in the lab, suggests a striking
similarity between telomeres and common fragile sites, parts of the genome where breaks
tend to occur, albeit infrequently. (Humans have 80 common fragile sites, many of which
have been linked to cancer.) De Lange and Sfeir found that these newly discovered fragile
sites make it difficult for DNA replication to proceed, a discovery that unveils a new
replication problem posed by telomeres.At the center of the discovery is a protein known
as TRF1, which de Lange, in an effort to understand how telomeres protect chromosome ends,
discovered in 1995. Using a conditional mouse knockout, de Lange and Sfeir have now
revealed that TRF1, which is part of a six-protein complex called shelterin, enables DNA
replication to drive smoothly through telomeres with the aid of two other proteins.
How toxins in the world are
killing us? Full Version
We are so focused on the Green
Movement, Global Warming, etc....but what about our own bodies. Now don't get me wrong -
we do need to work at creating better environments and doing what we can to save the
planet, but have you taken a look at the damage the world's toxins are doing to your own
body - even your children? How are these toxins affecting our daily lives? Should we worry
about toxins in the environment and how they could affect our bodies? Look around you
Children suffer from Cancer, Diabetes, ADD, AD/HD, obesity, Asthma, Autism to name a few.
Adults and elderly are even worse off. Every day we hear of yet another person in our
circle of influence whos been diagnosed with Cancer, MS, Fibromyalgia, Chronic Fatigue
Syndrome along with hundreds of other diseases. Since people are taking ownership of their
health and becoming partners with their physicians, detoxification has become the primary
method of prevention. Instead of waiting for something bad to happen and having to go to
the doctor, people are more proactive than ever before. This trend is recurring none too
soon, because so many people are getting sick! An important part of understanding how to
restore and protect our health is becoming informed about how toxic our environment is and
how that impacts good health. Were surrounded constantly by
environmental toxins and pollutants. Chemicals and heavy metals are prevalent in skin care
products; inside air is 1,000 times more toxic than outside air, foods are loaded with
herbicides, pesticides and chemicals. Even medications intended to help us are comprised
of toxic chemicals
The McDougall Diet/Autism
Connection
Is there a connection between diet and
autism? Hear what Dr. John McDougall and Barrie Silberberg have to say about the effects
of diet and autism.
If you read the previous chapter youre
already sold on the connections among autism, food intolerances and digestive complaints.
You also know enzyme therapy can be amazingly effective. Researchers also see deficient
enzyme levels in patients who have cancer, diabetes, heart disease, arthritis and other
diseases associated with aging and physical degeneration. Its a statistical fact that your
risk of all these diseases goes up as you age. Theyre nutritional deficiency diseases, at
least in part, just as surely as scurvy is a deficiency disease caused by lack of vitamin
C. If youve read this far, youve encountered a wealth of clinical evidence that proves
enzymes can slow or even reverse these diseases of age and degeneration. Enzymes belong in
your supplement cabinet, along with antioxidants, vitamins, minerals and the growing
number of plant compounds and chemicals that science has proven to promote good health.
Watch health Expert Byron J. Richards
describe potential health problems caused by poor dental hygiene and gum problems.
Children's Hospital of Pittsburgh
of UPMC scientists identify enzyme important in aging
The secret to longevity may lie in an enzyme with the ability to promote a robust immune
system into old age by maintaining the function of the thymus throughout life, according
to researchers studying an "anti-aging" mouse model that lives longer than a
typical mouse. The study, led by Abbe de Vallejo, Ph.D., associate professor of pediatrics
and immunology, University of Pittsburgh School of Medicine, and immunologist at
Children's Hospital of Pittsburgh of UPMC, reports that the novel mouse model has a thymus
that remains intact throughout its life. In all mammals, the thymus?the organ that
produces T cells to fight disease and infection?degenerates with age. Results of the study
are published in this week's issue of the Proceedings of the National Academy of Sciences.
"These findings give us hope that we may one day have the ability to restore the
function of the thymus in old age, or perhaps by intervening at an early age, we may be
able to delay or even prevent the degeneration of the thymus in order to maintain our
immune defenses throughout life," said Dr. de Vallejo.
Environmental manganese good in
trace amounts but can correlate to cancer rates
In the first ecological study of its kind in the world, a Wake Forest University Baptist
Medical Center researcher has uncovered the unique finding that groundwater and airborne
manganese in North Carolina correlates with cancer mortality at the county level. The
study, titled, "Environmental Manganese and Cancer Mortality Rates by County in North
Carolina: An Ecological Study," was published online last month by Biological Trace
Element Research. Lead researcher John Spangler, M.D., professor of family and community
medicine at Wake Forest Baptist, found that groundwater manganese appears to be positively
associated with total cancer, colon cancer and lung cancer death rates, while airborne
manganese concentrations appear to be inversely associated with total cancer, breast
cancer and lung cancer death rates. "People need manganese in trace amounts, but if
you get too much of it, manganese can be dangerous," Spangler said. "It's my
hope that the impact of this study will be to spark additional interest and research. This
really just raises the concern that something may be going on and argues for further
research into these issues." To determine whether environmental manganese is related
to cancer at the county level in North Carolina, Spangler conducted an ecological study
using data from the North Carolina State Center for Health Statistics, North Carolina
Geological Survey, U.S. Geological Survey, and U.S. Census. He found that airborne
manganese was associated at the county level with an 14 percent decrease in total cancer
deaths, a 43 percent decrease in breast cancer deaths and a 22 percent decrease in lung
cancer deaths. Additionally, Spangler found there was up to a 28 percent increase in
county-level colon cancer deaths and a 26 percent increase in lung cancer deaths at the
county level related to elevation of manganese in groundwater as opposed to air.
Losing sight of people in a crowd
can spell disaster, warns new report
Focusing on technology instead of people is a key factor in events going wrong, according
to a major series of reports into crowd behaviour and management, published this week.
Compiled for the Cabinet Office by researchers from two centres within Leeds University
Business School (COSLAC and CSTSD), the reports also claim that over-reliance on technical
and IT solutions means we fail to learn the lessons from past disasters. The Understanding
Crowd Behaviours reports are the first to bring together sociological and psychological
research on events and crowd behaviour, reviewing over 550 academic papers and drawing on
in-depth interviews with 27 specialists in the field (police, emergency planners and event
managers) to produce detailed guidelines for event organisers. The findings will be of use
to all those managing events involving large numbers of people and are particularly timely
in the run up to 2012.
New oral agents may prevent injury
after radiation exposure
Researchers from Boston University School of Medicine (BUSM) and collaborators have
discovered and analyzed several new compounds, collectively called the ''EUK-400 series,''
which could someday be used to prevent radiation-induced injuries to kidneys, lungs, skin,
intestinal tract and brains of radiological terrorism victims. The findings, which appear
in the June issue of the Journal of Biological Inorganic Chemistry, describe new agents
which can be given orally in pill form, which would more expedient in an emergency
situation. These agents are novel synthetic "antioxidants" that protect tissues
against the kind of damage caused by agents such as "free radicals." Free
radicals, and similar toxic byproducts formed in the body, are implicated in many
different types of tissue injury, including those caused by radiation exposure. Often,
this kind of injury occurs months to years after radiation exposure. The BUSM researchers
and their colleagues are developing agents that prevent injury even when given after the
radiation exposure. This paper describes a newer class of compounds, the ''EUK-400
series,'' that are designed to be given as a pill. According to the researchers,
experiments described in their paper prove that these agents are orally active. They also
show that the new agents have several desirable "antioxidant" activities, and
protect cells in a "cell death" model. These same BUSM researchers and
collaborators had previously discovered novel synthetic antioxidants that effectively
mitigate radiation injuries, but had to be given by injection. "We have developed
some of these agents and have studied them for over 15 years beginning with our work at
the local biotechnology company Eukarion," said senior author Susan Doctrow, PhD, a
research associate professor of medicine at BUSM's Pulmonary Center. "These
injectible antioxidants are very effective, but there has also been a desire to have
agents that can be given orally. A pill would be more feasible than an injection to treat
large numbers of people in an emergency scenario," she adds.
Digging in Beach Sand Increases
Risk of Gastrointestinal Illness
Children and adults who build castles and dig in the sand at the beach are at greater risk
of developing gastrointestinal diseases and diarrhea than people who only walk on the
shore or swim in the surf, according to researchers from the University of North Carolina
at Chapel Hill and the Environmental Protection Agency. People who playfully bury their
bodies in the sand are at even greater risk, according to the study published online
recently in the American Journal of Epidemiology. It also shows children, who are more
likely than adults to play with and possibly get sand in their mouths, stand the greatest
chance of becoming ill after a day at the beach. “Beach sand can contain indicators
of fecal contamination, but we haven’t understood what that means for people playing
in the sand,” said Chris Heaney, Ph.D., a postdoctoral epidemiology student at
UNC’s Gillings School of Global Public Health and lead author of the study.
“This is one of the first studies to show an association between specific sand
contact activities and illnesses.”The study is based on interviews with more than
27,000 people who visited seven freshwater and marine beaches in the agency’s
National Epidemiological and Environmental Assessment of Recreational Water Study (NEEAR)
between 2003 and 2005 as well as in 2007. All beaches in the study had sewage treatment
plant discharges within seven miles, although the source of sand pollution was unknown and
could have included urban runoff as well as wild and domestic animal contamination. Water
quality at the beaches was within acceptable limits, Heaney said.
Nicotine Induces Prediabetes,
Likely Contributes to High Prevalence of Heart Disease in Smokers
Researchers have discovered a reason why smoking greatly increases the risk of heart
disease and stroke. Nicotine promotes insulin resistance, also called prediabetes, which
is a risk factor for cardiovascular disease, according to the new study, which was
presented at The Endocrine Society’s 91st Annual Meeting in Washington, D.C.
Additionally, the study authors were able to partially reverse this harmful effect of
nicotine in mice by treating them with the nicotine antagonist mecamylamine, a drug that
blunts the action of nicotine. The study, which the National Institutes of Health funded,
was conducted by researchers at Charles Drew University of Medicine and Science in Los
Angeles and Western University of Health Sciences in Pomona, Calif.Their results may
explain why cigarette smokers have a high cardiovascular death rate, even though
“smoking causes weight loss, which should protect against heart disease,” said
the study’s lead author, Theodore Friedman, MD, PhD, chief of the endocrinology
division at Charles Drew University. Prediabetes and diabetes are known risk factors for
cardiovascular disease. Past studies show that cigarette smokers tend to be insulin
resistant, meaning that their hormone insulin does not work properly. To compensate, their
blood glucose (sugar) levels become higher than normal but not yet high enough for
diabetes. Smokers also have higher rates of diabetes, but it is not clear whether smoking
is the cause, because they could have other risk factors, Friedman explained.Some studies
demonstrate that nicotine and cigarette smoking induce high levels of the stress hormone
cortisol. “As cortisol excess is known to induce insulin resistance, it has been
suggested that glucocorticoids, such as cortisol, are the missing [causative] link between
cigarette smoking and insulin resistance,” Friedman said. The new study results
suggest this theory is correct, he said. The researchers studied the effects, on 24 adult
mice, of twice-daily injections of nicotine for 2 weeks. The mice ate less food than
control mice that received injections without nicotine, and they also lost weight and had
less fat. Despite this, the mice receiving nicotine developed prediabetes (insulin
resistance), which subsequent mecamylamine treatment improved somewhat. These mice also
had high cortisol levels in their blood and tissues, and mecamylamine blocked this
effect.“Our results suggest that reducing tissue glucocorticoid levels or decreasing
insulin resistance may reduce the heart disease seen in smokers,” Friedman said.
“We anticipate that in the future there will be drugs to specifically block the
effect of nicotine on glucocorticoids and insulin resistance.”
Mount Sinai researchers find new
Alzheimer's disease treatment promising
Researchers at Mount Sinai School of Medicine have found that a compound called NIC5-15,
might be a safe and effective treatment to stabilize cognitive performance in patients
with mild to moderate Alzheimer's disease. The two investigators, Giulio Maria Pasinetti,
M.D., Ph.D. , and Hillel Grossman, M.D., presented Phase IIA preliminary clinical findings
at the Alzheimer's Association 2009 International Conference on Alzheimer's Disease (ICAD)
in Vienna on Sunday, July 12. NIC5-15's potential to preserve cognitive performance will
be further evaluated in a Phase IIB clinical trial. Early evidence suggests that NIC5-15
is a safe and tolerable natural compound that may reduce the progression of Alzheimer's
disease-related dementia by preventing the formation of beta-amyloid plaque, a waxy
substance that accumulates between brain cells and impacts cognitive function. "With
Alzheimer's disease affecting 5.2 million Americans, another 5 million with early-state
disease, and nearly a half million new cases reported annually, treatments like NIC5-15
would make a significant difference in the lives of many Alzheimer's patients," said
Dr. Pasinetti, Professor of Psychiatry, Professor of Neuroscience and Professor of
Geriatrics and Adult Development, in the Department of Psychiatry at Mount Sinai School of
Medicine. "We are hopeful that the follow up clinical study will support this
preliminary evidence."
Excellent Prognosis for Prostate
Cancer Patients Treated with Brachytherapy
Prostate cancer patients who receive brachytherapy and were cancer-free for five years or
longer had a 97 percent chance of remaining cancer-free a decade after undergoing
treatment. The new study, conducted by Mount Sinai School of Medicine researchers, is
published in the July 1 issue of the International Journal of Radiation Oncology *Biology*
Physics, the official journal of the American Society for Radiation Oncology (ASTRO). The
lead author was Richard Stock, MD, Professor and Chair of Radiation Oncology at Mount
Sinai School of Medicine. Nelson Stone, MD, Clinical Professor of Urology, Oncological
Sciences and Radiation Oncology at Mount Sinai School of Medicine, served as a co-author.
Results from trials of DHA in
Alzheimer's disease and age-related cognitive decline
Results from two large studies using DHA, an omega 3 fatty acid, were reported today at
the Alzheimer's Association 2009 International Conference on Alzheimer's Disease (ICAD
2009) in Vienna. One of the trials was conducted by the Alzheimer's Disease Cooperative
Study (ADCS) supported by the National Institute on Aging (NIA), and the second by Martek
Biosciences Corporation (Martek), the primary company that makes algal DHA for
supplementation. The NIA trial lasted 18 months and was conducted in people with mild to
moderate Alzheimer's. Martek's trial was six months, and the compound was tested in
healthy people to see its effect on "age related cognitive decline" (ARCD). Both
studies used Martek's algal DHA. The results of the ADCS trial show no evidence for
benefit in the studied population. The Martek trial showed a positive result on one test
of memory and learning, but that study was in healthy older adults, not people with
Alzheimer's or another dementia. The results need confirmation, as is standard scientific
practice. "These two studies – and other recent Alzheimer's therapy trials
– raise the possibility that treatments for Alzheimer's must be given very early in
the disease for them to be truly effective," said William Thies, PhD, Chief Medical
& Scientific Officer at the Alzheimer's Association. "For that to happen, we need
to get much better at early detection and diagnosis of Alzheimer's, in order to test
therapies at earlier stages of the disease and enable earlier intervention." Other
research studies from ICAD 2009 show advances made in biomarkers and early detection from
the Alzheimer's Disease Neuroimaging Initiative (ADNI), and also survey results from
doctors about the enablers and barriers they face in diagnosing people with Alzheimer's.
DHA (docosahexaenoic acid) is naturally found in the body in small amounts, and is the
most abundant omega 3 fatty acid in the brain. DHA oil is abundant in some marine
microalgae, which provide the DHA that makes fatty fish a good source of DHA. Dietary DHA
is also available in foods enriched with algal DHA or fish oils, and dietary supplements.
Previous animal studies and epidemiology in humans suggested that DHA may be beneficial in
people with Alzheimer's.
Dinosaur Burrow Find Gives Climate
Change Clues
On the heels of his discovery in Montana of the first trace fossil of a dinosaur burrow,
Emory University paleontologist Anthony Martin has found evidence of more dinosaur burrows
– this time on the other side of the world, in Victoria, Australia. The find, to be
published this month in Cretaceous Research, suggests that burrowing behaviors were shared
by dinosaurs of different species, in different hemispheres, and spanned millions of years
during the Cretaceous Period, when some dinosaurs lived in polar environments.
Ozone, nitrogen change the way
rising CO2 affects Earth's water
Through a recent modeling experiment, a team of NASA-funded researchers have found that
future concentrations of carbon dioxide and ozone in the atmosphere and of nitrogen in the
soil are likely to have an important but overlooked effect on the cycling of water from
sky to land to waterways. The researchers concluded that models of climate change may be
underestimating how much water is likely to run off the land and back into the sea as
atmospheric chemistry changes. Runoff may be as much as 17 percent higher in forests of
the eastern United States when models account for changes in soil nitrogen levels and
atmospheric ozone exposure. "Failure to consider the effects of nitrogen limitation
and ozone on photosynthesis can lead us to underestimate regional runoff," said
Benjamin Felzer, an ecosystem modeler at Lehigh University in Bethlehem, Pa. "More
runoff could mean more contamination and flooding of our waterways. It could also mean
fewer droughts than predicted for some areas and more water available for human
consumption and farming. Either way, water resource managers need more accurate runoff
estimates to plan better for the changes." Felzer and colleagues from the
Massachusetts Institute of Technology (MIT) in Cambridge and the Marine Biology Laboratory
in Woods Hole, Mass., published their findings recently in the Journal of Geophysical
Research – Biogeosciences. Plants play a significant role in Earth's water cycle,
regulating the amount of water cycling through land ecosystems and how long it stays
there. Plants draw in water from the atmosphere and soil, and they discharge it naturally
through transpiration, the tail end of photosynthesis when water vapor and oxygen are
released into the air. The amount of water that plants give up depends on how much carbon
dioxide is present in the atmosphere. Studies have shown that despite a global drop in
rainfall over land in the past 50 years, runoff has actually increased. Other studies have
shown that increasing CO2 is changing how plant "pores," or stomata, discharge
water. With elevated CO2 levels, leaf pores contract and sometimes close to conserve
internal water reserves. This "stomatal conductance" response increases water
use efficiency and reduces the rate of transpiration.
Toward an explanation for Crohn's
disease?
Twenty-five per cent of Crohn's disease patients have a mutation in what is called the
NOD2 gene, but it is not precisely known how this mutation influences the disease. The
latest study by Dr. Marcel Behr, of the Research Institute of the MUHC and McGill
University, has provided new insight into how this might occur. The study will be
published on July 9th in the Journal of Experimental Medicine. When the NOD2 gene
functions normally, it codes for a receptor that will recognize invading bacteria and then
trigger the immune response. This study demonstrates that the NOD2 receptor preferentially
recognizes a peptide called N-glycolyl-MDP, which is only found in a specific family of
bacteria called mycobacteria. When mycobacteria invade the human body, they cause an
immediate and very strong immune response via the NOD2 receptor. "Now that we have a
better understanding of the normal role of NOD2, we think that a mutation in this gene
prevents mycobacteria from being properly recognized by the immune system," explained
Dr. Behr. "If mycobacteria are not recognized, the body cannot effectively fight them
off and then becomes persistently infected." Researchers were already aware of the
relationship between mycobacteria and Crohn's disease, but they did not know whether the
presence of bacteria was a cause or a consequence of the disease. This new discovery
associates the predisposition for Crohn's disease with both the NOD2 mutation and the
presence of mycobacteria, but researchers must still determine the precise combination of
these factors to understand how the disease develops. More research is required to
establish a complete explanation. From this, it is expected that new therapeutic
approaches that fight the cause of Crohn's disease may be developed
Novel genetic finding offers new
avenue for future Crohn's disease treatment
Researchers from Case Western Reserve University School of Medicine identified a novel
link between ITCH, a gene known to regulate inflammation in the body and NOD2, a gene
which causes the majority of genetic Crohn's Disease diagnoses. ITCH, when malfunctioning,
causes widespread inflammatory diseases, including inflammatory bowel disease, gastritis,
uncontrolled skin inflammation, and pulmonary pneumonitis. Derek Abbott, M.D., Ph.D., and
his team of researchers found that ITCH also influences NOD2-induced inflammation. These
findings, published in the August 11th issue of Current Biology, suggest a common
pathophysiology exists between multiple inflammatory diseases. The unexpected finding of
the interaction between these genes offers the possibility of a new drug target, which
would be effective in treating Crohn's disease – a chronic disorder causing
inflammation of the gastrointestinal tract. Autoimmune and inflammatory diseases are
striking an increasing portion of the population. They result from an overstimulation of
the immune system by the infectious and environmental agents individuals face daily.
Unfortunately, despite their increasing prevalence in the Western world and morbidity
among younger patients, the pathophysiology of these enigmatic diseases is poorly
understood and for this reason, treatment for these diseases is less-than-ideal. This
finding links two key signaling pathways to the pathophysiology of diseases associated
with ITCH and NOD2 and opens new avenues of pharmacologic pursuit to target these
diseases. With an eye towards clinical applications, Dr. Abbott and his colleagues' next
step is to determine if currently used pharmacologic agents can be useful in this model of
inflammatory disease. They will do so using small molecule drug screening to identify
potential drugs that target ITCH.
Study identifies potential fix for
damaged knees
Investigators from Hospital for Special Surgery have shown that a biodegradable scaffold
or plug can be used to treat patients with damaged knee cartilage. The study is unique in
that it used serial magnetic resonance imaging (MRI) and newer quantitative T2 mapping to
examine how the plug incorporated itself into the knee. The research, abstract 8372, will
be presented during the annual meeting of the American Orthopedic Society for Sports
Medicine, June 9-12, in Keystone, Colo. "The data has been encouraging to support
further evaluation of this synthetic scaffold as a cartilage repair technique," said
Asheesh Bedi, M.D., a fellow in sports medicine and shoulder surgery at Hospital for
Special Surgery who was involved with the study. Dr. Bedi performed analysis of MRI scans
of patients primarily treated by Riley Williams, M.D., director of the Institute for
Cartilage Repair at Hospital for Special Surgery. "The Trufit plug has been designed
to have mechanical properties that are similar to cartilage and bone," Dr. Bedi said.
Damage to so-called articular cartilage can occur in various ways, ranging from direct
trauma in a motor vehicle accident to a noncontact, pivoting event on the soccer field.
"Articular cartilage lacks the intrinsic properties of healing—you are
essentially born with the articular cartilage that you have," Dr. Bedi said. Left
untreated, these injuries can increase loads placed on the remaining intact cartilage and
increase the risk of progression to degenerative arthritis. One way to treat patients with
symptomatic chondral lesions is an OATS procedure, in which cartilage is transferred from
one portion of the knee to treat another. Because this is a "robbing Peter to pay
Paul" situation, researchers at Hospital for Special Surgery set out to examine
whether they could use a biodegradable plug, the Trufit CB plug, to fill the donor site.
The goal was to monitor how the plug incorporated itself into the knee and to evaluate the
quality of the repair cartilage. The Trufit plug has two layers. The top layer has
properties similar to cartilage and the lower layer has properties similar to bone. The
bilayered structure has mechanical properties that approximately match the adjacent
cartilage and bone. Surgeons inserted the plug in the knees of 26 patients with donor
lesions from OATS procedures and followed up with imaging studies (with MRI and
T2-mapping) at various intervals for a period of 39 months."Quantitative MRI, when
combined with morphologic assessment, allows us to understand the natural history of these
repair techniques and define those patients who are most likely to benefit from the
surgery," said Hollis Potter, M.D., chief of the Division of Magnetic Resonance
Imaging, director of Research in the Department of Radiology and Imaging at Hospital for
Special Surgery and lead author of the study. "We gain knowledge about the biology of
integration with the host tissue, as well as the repair tissue biochemistry, all by a
noninvasive imaging technique."
Newborn brain cells show the way
Although the fact that we generate new brain cells throughout life is no longer disputed,
their purpose has been the topic of much debate. Now, an international collaboration of
researchers made a big leap forward in understanding what all these newborn neurons might
actually do. Their study, published in the July 10, 2009, issue of the journal Science,
illustrates how these young cells improve our ability to navigate our environment.
"We believe that new brain cells help us to distinguish between memories that are
closely related in space," says senior author Fred H. Gage, Ph.D., a professor in the
Laboratory for Genetics at the Salk Institute and the Vi and John Adler Chair for Research
on Age-Related Neurodegenerative Diseases, who co-directed the study with Timothy J.
Bussey, Ph.D., a senior lecturer in the Department of Experimental Psychology at the
University of Cambridge, UK, and Roger A. Barker, PhD., honorary consultant in Neurology
at Addenbrookes Hospital and Lecturer at the University of Cambridge. When the first clues
emerged that adult human brains continually sprout new neurons, one of the central tenets
of neuroscience—we are born with all the brain cells we'll ever have—was about
to be overturned. Although it is never easy to shift a paradigm, a decade later the
question is no longer whether neurogenesis exists but rather what all these new cells are
actually good for. "Adding new neurons could be a very problematic process if they
don't integrate properly into the existing neural circuitry," says Gage. "There
must be a clear benefit to outweigh the potential risk."
Reduced diet thwarts aging, disease
in monkeys
The bottom-line message from a decades-long study of monkeys on a restricted diet is
simple: Consuming fewer calories leads to a longer, healthier life. A team of researchers
at the University of Wisconsin-Madison, the Wisconsin National Primate Research Center and
the William S. Middleton Memorial Veterans Hospital reports that a nutritious but
reduced-calorie diet blunts aging and significantly delays the onset of such age-related
disorders as cancer, diabetes, cardiovascular disease and brain atrophy. "We have
been able to show that caloric restriction can slow the aging process in a primate
species," says Richard Weindruch, a professor of medicine in the UW-Madison School of
Medicine and Public Health who leads the National Institute on Aging-funded study.
"We observed that caloric restriction reduced the risk of developing an age-related
disease by a factor of three and increased survival." During the 20-year course of
the study, half of the animals permitted to eat freely have survived, while 80 percent of
the monkeys given the same diet, but with 30 percent fewer calories, are still alive.
Begun in 1989 with a cohort of 30 monkeys to chart the health effects of the
reduced-calorie diet, the study expanded in 1994 with the addition of 46 more rhesus
macaques. All of the animals in the study were enrolled as adults at ages ranging from 7
to 14 years. Today, 33 animals remain in the study. Of those, 13 are given free rein at
the dinner table, and 20 are on a calorie-restricted diet. Rhesus macaques have an average
life span of about 27 years in captivity. The oldest animal currently in the study is 29
years. The new report details the relationship between diet and aging, according to
Weindruch and lead study author Ricki Colman, by focusing on the "bottom-line
indicators of aging: the occurrence of age-associated disease and death."
2 reproductive factors are
important predictors of death from ovarian cancer
Researchers from the Centers for Disease Control and Prevention (CDC) found that survival
among women with ovarian cancer is influenced by age of menarche and total number of
lifetime ovulatory cycles. This finding suggests that hormonal activity over the course of
a woman's lifetime may influence the prognosis after an ovarian cancer diagnosis. Results
of this study are published in Cancer Epidemiology, Biomarkers & Prevention, a journal
of the American Association for Cancer Research. Results of previous studies indicated
that fewer lifetime ovulatory cycles, higher parity, oral contraceptive use, hysterectomy
and tubal ligation are associated with decreased risk of developing this form of cancer,
according to the researchers. However, little is known about the influence of these
factors on a patient's survival after a diagnosis of ovarian cancer. Cheryl L. Robbins,
Ph.D., an epidemiologist at the CDC, and colleagues sought to explore whether these
reproductive factors influence ovarian cancer survival. "Ovarian cancer is the fifth
leading cause of cancer mortality in women. It accounts for more deaths than any other
gynecologic cancer," said Robbins, also a researcher on the study. "Although we
have relatively good knowledge about the influence of reproductive factors on the risk of
developing ovarian cancer, knowledge is rather limited regarding the reproductive factors
that may influence survival after diagnosis with this serious disease."Robbins and
colleagues conducted a longitudinal analysis of 410 women, aged 20 to 54 years. All
participants were previously enrolled in the 1980-1982 Cancer and Steroid Hormone (CASH)
study as incident ovarian cancer cases. After a follow-up of about 17 years, 221 women
died; findings showed that overall 15-year survival among the study population was 48
percent. Lifetime ovulatory cycle and age at menarche were two factors that played a key
role in predicting death from ovarian cancer. Women with the most lifetime ovulatory
cycles had poorer survival compared with those who had fewer lifetime ovulatory cycles.
Robbins explained that the number of lifetime ovulatory cycles a woman has is affected by
her use of oral contraceptives, pregnancy and breastfeeding, all of which temporarily
cause ovulation to cease and reduces the total number of cycles. Furthermore, the
researchers determined that those with the youngest age at menarche also had poorer
survival. After diagnosis of ovarian cancer, participants whose menarche began before age
12 were more likely to die compared with those whose menarche began at age 14 or older.
"We now have evidence that higher numbers of lifetime ovulatory cycles may play a
role in the development of ovarian cancer as well as the risk of death after being
diagnosed with the disease," Robbins concluded.
Link Between Migraines and Reduced
Breast Cancer Risk Confirmed in Follow-Up Study
The relationship between migraine headaches in women and a significant reduction in breast
cancer risk has been confirmed in a follow-up study to landmark research published last
year. Results of this new study showed a 26 percent reduced risk of breast cancer among
premenopausal and postmenopausal women with a clinical diagnosis of migraines. The study
appears in the July issue of Cancer Epidemiology, Biomarkers & Prevention, a journal
of the American Association for Cancer Research. Christopher I. Li, M.D., Ph.D., led the
first-of-its-kind study linking migraines with breast cancer risk reduction, which was
published in the same journal last November. Li is a breast-cancer epidemiologist and
associate member of the Fred Hutchinson Cancer Research Center's Public Health Sciences
Division, in Seattle. This time, Li and colleagues found that the risk reduction remained
statistically similar regardless of a woman's menopausal status, her age at migraine
diagnosis, use of prescription migraine medications or whether she avoided known migraine
"triggers" such as alcohol consumption, smoking and taking hormone replacement.
These triggers are also well-established breast cancer risk factors.
