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Cholesterol-lowering drugs and the risk of hemorrhagic stroke

Contact: Angela Babb
ababb@aan.com
651-695-2789
American Academy of Neurology

ST. PAUL, Minn. – People taking cholesterol-lowering drugs such as atorvastatin after a stroke may be at an increased risk of hemorrhagic stroke, or bleeding in the brain, a risk not found in patients taking statins who have never had a stroke. But researchers caution the risk must be balanced against the much larger overall benefit of the statin in reducing the total risk of a second stroke and other cardiovascular events when making treatment decisions. The research is published in the December 12, 2007, online issue of Neurology®, the medical journal of the American Academy of Neurology.

For the study, researchers conducted a secondary analysis of the results of the Stroke Prevention with Aggressive Reduction in Cholesterol Levels (SPARCL) clinical trial. The trial enrolled 4,731 people who were within one to six months of having had a stroke or transient ischemic attack, or mini-stroke, and with no history of heart disease. Half of the participants received atorvastatin and half received a placebo. The participants were then followed for an average of four and a half years.

Overall, treatment was associated with a 16-percent reduction in total stroke, the study’s primary endpoint, as well as significant reductions in coronary heart events. However, secondary analysis found that the overall reduction in stroke included an increase in the risk of brain hemorrhage. Of those people randomized to atorvastatin, the study found 2.3 percent experienced a hemorrhagic stroke during the study compared to 1.4 percent of those taking placebo. The study also found there was a 21-percent reduction in ischemic stroke, a more common type of stroke involving a block in the blood supply to the brain, among people taking atorvastatin.

Other factors were also found to increase the risk of brain hemorrhage. For example, those who had experienced a hemorrhagic stroke prior to the study were more than five times as likely to suffer a second stroke of this kind. Men were also nearly twice as likely as women to suffer a hemorrhagic stroke. People with severe high blood pressure at their last doctor’s visit prior to the hemorrhagic stroke had over six times the risk of those with normal blood pressure.

“Although treatment of patients with a stroke or transient ischemic attack was clearly associated with an overall reduction in a second stroke, hemorrhagic stroke was more frequent in people treated with atorvastatin, in those with a prior hemorrhagic stroke, in men and in those with uncontrolled hypertension,” according to study author Larry B. Goldstein, MD, with Duke University Medical Center in Durham, North Carolina, and Fellow of the American Academy of Neurology. “This risk of hemorrhagic stroke also increased with age.”

“Treatment with atorvastatin did not disproportionately increase the frequency of brain hemorrhage associated with these other factors. The risk of hemorrhage in patients who have had a transient ischemic attack or stroke must be balanced against the benefits of cholesterol-lowering drugs in reducing the overall risk of a second stroke, as well as other cardiovascular events,” said Goldstein.

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The SPARCL trial was funded by Pfizer, the maker of atorvastatin.

The American Academy of Neurology, an association of more than 20,000 neurologists and neuroscience professionals, is dedicated to improving patient care through education and research. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as stroke, Alzheimer’s disease, epilepsy, Parkinson disease, and multiple sclerosis.

For more information about the American Academy of Neurology, visit http://www.aan.com.

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December 13, 2007 Posted by | American Academy of Neurology, Baltimore, Barcelona, Bethesda, Boston, Calgary, Canada, FMS Global News, France, Germany, Global, Global Health Vision, Global News, Hemorrhagic Stroke, Italy, London, London UK Feed, Medical Journals, Newfoundland, News, News Australia, News Canada, News France, News Germany, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, Nova Scotia, Ottawa, Ottawa City Feed, Quebec, Research, RSS Feed, Slovakia, Spain, Statin Drugs, Stroke, Toronto, Toronto City Feed, UK, US, Virginia, Washington DC, Washington DC City Feed, World News | , , | Leave a comment

FOOD FOR SKINNY KIDS – A STORY WHICH NEEDS TO CIRCULATE FOREVER

by Jeanne Hambleton © 2007
NFA Leader Against Pain – Advocate

Maybe I should mention that you just might need some kleenex tissues before you start this story but please read it anyway, if only in the spirit of Goodwill to All Children. The men are big enough to look after themselves.

As folks in the UK were getting ready this morning to do some Christmas shopping an email arrived on my desktop with a warning, which said,  “This email needs to circulate forever.”

How could I pass up this invitation to inquire within? The email also stated, “This is a real eye opener. A real tear jerker No prerequisites (commitments).  Simply, because everyone should be reminded.“

This was sent to me by a lady from Montevideo, Uruguay called Marta. Where the pictures, shown in the email, were taken, it does not say, but I am sure it conveys a worldwide message, especially within the African continent.

Picture 1. shows European students sat at computers working, with the caption, “Does studying annoy you?”
Picture 2. reveals children, possibly from Africa, without shoes, sat on a bench and drawing their lessons in the dirt with their fingers. The caption says, “ Not them!”


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Picture 3. is a happy family picture of a father with his daughter enjoying a beef burger roll with the words, “Hate veggies?”
Picture 4. is a picture of a long line of native mothers and starved children, clothed, in rags and waiting in line with a bowl for some food handouts. This caption says, “They starve from hunger!”


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Picture 5. reveals the back view of a jolly obese child having fun, with a caption which reads, “On a diet?”
Picture 6. gives a close-up of a painfully thin starved child with a tape measure around the child’s matchstick thin arm. The caption referring to diet says, “They die from it!” Or the lack of any kind of diet.


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Picture 7. shows a baby being cuddled by a parent revealing the lovely cuddly cheeks of a child’s bottom. This reads, “Does your parent’s care tire you?”
Picture 8. shows a sibling cuddling a child with the last bone in the baby’s spine clearly visible as she rests in sister’s arms for comfort. This caption tells us these children have no parents to grow tired of. “They don’t have any!”


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Picture 9. reveals youngsters sat at a games console and states, “Bored with the same game?”
Picture 10. Shows a young unclothed child playing in the dirt with a bit of stick, next to the human skull of someone who had probably died from starvation. The caption reads, “They have no option!”


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Picture 11. shows a smart new trainer with a caption which reads, “Someone got you Adidas instead of Nike?”
Picture 12. pictures the feet of a child with half of a plastic bottle cut to make the sole of a pair of sandals. The picture clearly reveals the screw top of the plastic bottle on the footwear, which is tied onto the foot with rag. This caption states, “They only have one brand?” Maybe it is cola?????


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Picture 13. is of a sweet little girl in clean pyjamas snuggled up in her cosy bed. This caption reads, “Aren’t you thankful for a bed to sleep in?”
Picture 14. The final contrast picture shows a child laying in the dirt, half covered with a piece of old rag, trying to sleep, with a caption that reads, “They’d wish not to wake up!”


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The closing slide asks, “Are you still complaining? Observe around you and be thankful for all that you have in this transitory lifetime…. We are fortunate to have much more than what we need to be content. Let us try not to feed this endless cycle of consumerism and immortality in which this ‘modern and advanced’ society forgets and ignores the other two thirds of our brothers and sisters. Send this information without any obligation or expectation in receiving good luck. Don’t keep it! Send it and it won’t be in vain. Let us complain less and give more!”

I imagine you feel as I do. I work hard for my dollar and I do not believe in sharing my hard earned cash with large charities who have magnificent offices, managing directors, hundreds of paid staff and devote just a fraction of their donations to their ‘good’ works. You can call me the woman with the long pockets if you like, but I want to know my money is going where it will doing some good and helping those would really need it. How to be confident about that I am not sure? In true Scorpion fashion I hate to be misled or deceived.

Quite how we can help these starving children is the burning question. I have had masses of appeals for all sorts of charities drop on my doormat in recent weeks. At least these ends up in the local hospice waste paper recycling skip and help them a little along with our papers and magazines. I looked on the Internet at our UK BBC Children in Need but could not see children in a similar situation.

SAVE THE CHILDREN
The UK Save the Children organisation has produced a Christmas shopping catalogue, on line, so should you decide to buy Christmas gifts from them you are indirectly donating while shopping, just how much remains to be seen! Perhaps this might be more acceptable – buying and giving at the same time. It is easy to look at this site to see the work they are doing and possibly shop with them. Every Christmas I seem to receive more and more cards printed by charities and sent by to me by friends.

http://www.savethechildrenshop.co.uk/home

However I should mention that if you telephone their UK number – 0844 557 5425 – instead of ordering on line, it could cost you 40p a minute as you give your details and make your mind up. Some of that money will be going to the charity.

Our doctors’ surgery is using this 0844 prefix number and getting a rake off which is a bit vexing considering how much our GPs are reported to be earning – but that is another story.

No – I am not a sales rep for any charity – just a concerned parent. No, this is not a commercial for children’s charities – it is a wake up call.

The American Save the Children website also appears to have a programme for under privileged children in developing countries, who are suffering from hunger and poverty. It seems you can also purchase festive gifts from them indirectly helping the cause.

http://www.savethechildren.org/

What you decide to do is between you and your conscience. I would however like to leave you with these thoughts.

These pictures and words certainly do bring you down to earth especially when you consider the wastage by governments the world over.  I am just sorry I could not reproduce the pictures but I am sure you know the kind of scenes I mean – you must have seen them on TV from time to time. Send me your email address with the request for these pictures if you would like them forwarding.

Just consider the money all of the worldwide governments squander… it is time someone added the total figure and gave us some home truths.

These starving children, if they live, may be our next generation – our future leaders. Do you think if they survive they could be future terrorists? I am sure they will have a grudge against the world – surely they will feel the world owes them a living. This is all very sad and really makes you think. Whatever happened to the innocence of childhood?  

Just imagine what we spend on consumerism not to mention what we will spend on our own children this Christmas 2007. I wonder what our children would think if we put these pictures under the Christmas tree on Dec.25 instead of a new bike, a new game toy and all the other things children of our modern world expect to receive from their parents aka Father Christmas?

What would it be like if children all over the world went without just one toy from their festive gifts in aid of the starving and poverty stricken children. It would take a lot of organizing to gather in that money and it is a huge task but it could be done – all it needs is a good website supported by reliable well known people…. even if it took until Easter to collect the money – the children would still be starving.

Where are you Bob Geldorf? Can you help us with this? Does someone know his email address? My mind is boggling at the power of the people…… How about Skinny Kids for a campaign title – that rather sums it up!

Just a thought – maybe if that £5 we would be spending on a nonsense stocking gift for someone who has everything, was replaced with a warm note telling them Christmas is for children – starving children in particular – and they would be receiving his gift money with a tax gift aid. Sorry but this has been sent to starving “Skinny Kids” who have nothing.

I would hope we would get a really warm hug for this initiative. This friend really did not need an air freshener toy for his car or a key ring. If we did not get a big hug that receiver is a Christmas Meanie…. Take it from me. We will cross him off our Christmas list in future – so there.

Sorry to be a party pooper – but someone has to do it.  I will make up for it and send you some happier stories in the near future.

Take care. Jeanne.

November 26, 2007 Posted by | Childhood Nutrition, Global Health Vision, Global News, Health, Hunger, London UK Feed, News, News Australia, News Canada, News France, News Germany, News Israel, News Italy, News Switzerland, News UK, News US, News USA, Ottawa, Ottawa City Feed, RSS Feed, Toronto, Toronto City Feed, UK, Virginia, Washington DC, Washington DC City Feed, World News | , , | Leave a comment

Antibody leads to repair of myelin sheath in lab study of multiple sclerosis and related disorders

Contact: Amelyn Reyes
newsbureau@mayo.edu
507-284-5005
Mayo Clinic

ROCHESTER, Minn. — Mayo Clinic researchers have found that a human antibody administered in a single low dose in laboratory mouse models can repair myelin, the insulating covering of nerves that when damaged can lead to multiple sclerosis and other disorders of the central nervous system.

The study will be presented on Oct. 9 at the American Neurological Association meeting in Washington, D.C.

“The repair of chronic spinal cord injury is seldom modeled in laboratory studies, but it is an important reality for the treatment of humans. The concept of using natural human antibodies to treat disease of this kind has not yet been tested in humans, but these research findings are very promising,” says Moses Rodriguez, M.D., a Mayo Clinic neurologist and the study’s corresponding author. “The findings could eventually lead to new treatments that could limit permanent disability,” states Arthur Warrington, Ph.D., a Mayo Clinic scientist and study author.

Myelin repair normally occurs spontaneously, but in multiple sclerosis and other disorders of the central nervous system, the myelin repair process occurs very slowly or fails altogether. Researchers are trying to determine how to speed up the myelin healing process, which they hope will eventually lead to new treatments for patients.

The antibody, which was genetically engineered from a single cell, binds to myelin and the surface of cells in the brain and spinal cord, then it triggers the cells to begin the repair process called remyelination. This antibody is the first known reagent designed to induce repair by acting within the central nervous system at the damage sites on cells responsible for myelin synthesis.

The study uses laboratory mouse models of chronic progressive multiple sclerosis in humans. The severity of the disease and also success of the treatment were largely defined by how naturally active the mice were, particularly during the night because mice are nocturnal and are especially active at this time. They received a single dose of the antibody. A minimum of 25 mcg/kg was needed to trigger remyelination, which is equivalent to about 2 mg in the average adult, considered a very low dose. The myelin repair plateaued after five weeks in the mice models.

In addition, when combined with daily methylprednisolone, (an immune modulating steroid) the antibody still promotes remyelination in mouse models. This is an important fact because the first multiple sclerosis patients treated with the antibody will have been treated first with methylprednisolone.

As a naturally occurring protein of the immune system, antibodies do not appear to carry any side effects, nor are they toxic — even when administered at 4,000 times the minimal effective dose — though the concept has not yet been tested in humans, the researchers say.

In summary, this antibody:

Promotes remyelination with a single dose as low as 25 mcg/kg in mice models

The remyelination plateaus at five weeks after a single dose

Converts a model of chronic immune mediated demyelination to one that repairs with the speed of a toxin induced model of demyelination

In terms of replicating the findings in humans, the researchers have already produced the antibody through genetic engineering and conducted preliminary toxicology experiments in mice showing that 1,000 times the therapeutic dose is not toxic. The study continues to be explored in animal models and eventually, in clinical trials.

In short, the critical finding is that when combined with methylprednisolone, the antibody still effectively promotes remyelination and does not make the mice worse, Dr. Warrington states.

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About Multiple Sclerosis:

Multiple sclerosis (MS) is a chronic, potentially debilitating disease that affects the central nervous system, which is made up of the brain and spinal cord. Multiple sclerosis is widely believed to be an autoimmune disease, a condition in which the immune system attacks components of the body as if they’re foreign.

Multiple sclerosis affects an estimated 300,000 people in the United States and probably more than 1 million people around the world — including twice as many women as men. Most people experience their first signs or symptoms between ages 20 and 40.

Collaboration and Support

The study was funded by the National Institutes of Health, the National Multiple Sclerosis Society, Multiple Sclerosis Society of Canada, the Hilton Foundation and Mr. and Mrs. Eugene Applebaum.

To obtain the latest news releases from Mayo Clinic, go to http://www.mayoclinic.org/news. MayoClinic.com (www.mayoclinic.com) is available as a resource for your health stories. For more on Mayo Clinic research, go to http://www.mayo.edu.

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October 9, 2007 Posted by | Global Health Vision, Global News, Mayo Clinic, MS, Multiple Sclerosis, News, News USA, Ottawa, RSS Feed, Toronto, UK, Washington DC City Feed | 3 Comments

Medication appears helpful for treatment of erectile dysfunction in men with spinal cord injuries

The drug tadalafil appears to improve erectile function in men with spinal cord injuries, according to an article posted online today that will appear in the November 2007 print issue of Archives of Neurology, one of the JAMA/Archives journals.

Between 10.4 and 83 individuals per million worldwide experience spinal cord injuries every year, according to background information in the article. “Throughout the world, spinal cord injury occurs most often in young men, resulting in negative physical, social and psychological consequences,” the authors write. “Erectile dysfunction, defined as the inability to attain and maintain penile erection sufficient for satisfactory sexual performance, is a common complication in men with spinal cord injury.” Only 25 percent of men with spinal cord injuries are able to have erections that are adequate for having intercourse.

Francois Giuliano, M.D., Ph.D., of the Raymond Poincare Hospital, Garches, France, and colleagues, conducted a randomized, double-blind study of tadalafil in 197 men with spinal cord injuries (average age 38). After a four-week period during which none of the men received treatment, 142 were randomly assigned to the tadalafil treatment group and 44 to the placebo group. During the 12-week treatment phase, the participants were instructed to take the medication as needed before the potential for sexual activity, with a maximum of one dose daily. Those assigned to take tadalafil were given a 10-milligram dose at first and were evaluated every four weeks, at which time patients were switched to a 20-milligram dose based on their response to the treatment.

At the beginning of the study, the men’s average score on the International Index of Erectile Function—a 15-item questionnaire on which a score of 25 or lower indicates erectile dysfunction—was 13.4. After 12 weeks of treatment, men taking tadalafil had an average score of 22.6 (indicating mild erectile dysfunction) and men taking placebo had an average score of 13.6 (indicating moderate erectile dysfunction). Men taking tadalafil were, on average, successful 75.4 percent of the times they attempted penetration and 47.6 percent of the times they attempted intercourse, compared with a 41.1 success rate for penetration and 16.8 percent for intercourse among men taking placebo.

“Tadalafil was safe and well tolerated with few treatment-emergent side effects,” the authors write. Fifty (35 percent) of patients in the tadalafil group and 15 (34 percent) of those in the placebo group experienced at least one adverse effect. Among those taking tadalafil, the most common side effects were headache (8.5 percent of patients) and urinary tract infection (7.7 percent of patients).

“As in other erectile dysfunction studies that include patients who were difficult to treat owing to pre-existing conditions (e.g., prostatectomy, diabetes mellitus), tadalafil was efficacious for the treatment of erectile dysfunction after a traumatic spinal cord injury,” the authors write. “On-demand treatment with tadalafil (10 milligrams or 20 milligrams) may help improve the sex lives of patients with erectile dysfunction and spinal cord injury and their partners.”

(Arch Neurol. 2007;64(11):(doi:10.1001/archneur.64.11.nct70001). Available pre-embargo to the media at http://www.jamamedia.org.)

Editor’s Note: Funding for this study was provided by Lilly ICOS LLC, Bothell, Wash., and Indianapolis, Ind. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

Contact: Francois Giuliano, M.D., Ph.D.
giuliano@cyber-sante.org
JAMA and Archives Journals

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September 10, 2007 Posted by | Archives of Neurology, Global Health Vision, Global News, JAMA/Archives journals, RSS Feed, Science, Spinal Cord Injuries, UK, Washington DC City Feed | Leave a comment

New study highlights link between unemployment and hospital trauma admissions

Press Releases

Heidelberg, 8 August 2007

Unemployment cuts

Socioeconomic status, and unemployment rates in particular, predict both the type of trauma seen in emergency rooms and the population groups more likely to be victims of trauma, according to Atul Madan (1) from the University of Tennessee Health Science Center and his team. Their findings have just been published online in Springer’s World Journal of Surgery.

The researchers looked at the link between unemployment rates and the types of trauma admissions in New Orleans over six years. Unemployment rates were obtained from the Bureau of Labor Statistics. The trauma registry of the Medical Center of Louisiana at New Orleans (Charity Hospital) provided data on the trauma emergency room admissions, including patient demographics.

Between January 1994 and November 1999, there were over 24,000 trauma admissions. During that period, the higher the unemployment rate, the higher the number of admissions for penetrating trauma – injuries that occur primarily by an object piercing the skin or entering a tissue of the body, such as bullets and knives.

The lower the unemployment rates, the higher the number of admissions for blunt trauma – physical trauma caused to a body part, either by impact, injury of physical attack which can result in contusions, abrasions, lacerations and bone fractures. In this instance, the majority of blunt trauma was the result of motor vehicle collisions. The authors suggest that a possible explanation for this surprising finding could be the fact that with higher incomes, more travel is likely, which in turn increases the likelihood of motor vehicle collisions. Alternatively, more tourism to the area may have reduced unemployment but caused more road accidents.

The study also shows that as the socioeconomic status, measured here by unemployment rates, of the community changes, so do the demographics and mortality rates of the trauma population. There were more male patients, African American patients and deaths at times of high unemployment. These results suggest that during times of economic hardship, certain population groups are at higher risk of life-threatening injuries.

The authors recommend that “injury prevention efforts targeted at economically disadvantaged populations and high-risk groups should be stressed when designing community trauma outreach programs, especially during times of economic hardships.”

Reference
(1) Madan A et al (2007). Unemployment rates and trauma admissions. World Journal of Surgery (DOI 10.1007/s00268-007-9190-4)

Contact:
Renate Bayaz
tel +49-6221-487-8531

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August 8, 2007 Posted by | Canada, Global Health Vision, Global News, Health Canada, Hospital Trauma, Music Video Of The Day, News, News USA, Ottawa, RSS Feed, Toronto, UK, Unemployment, Virginia, Washington DC, Washington DC City Feed, World News | Leave a comment

A pioneering study opens roads for tailor-made antidepressants

In spite that the causes of depression have not still been fully identified, scientists acknowledge that genetic and environmental factors play a common role in the onset of this disorder. One of the environmental risk factors more often related to depression is exposure to threatening life events. On the other side, from a genetic point of view, the serotonin transporter gene, with a crucial role in communication between neurons, could predispose to depression.

An international group of scientists, headed by professors Jorge Cervilla Ballesteros and Blanca Gutiérrez Martínez, from the department of Legal Medicine, Toxicology and Psychiatry of the University of Granada, has recently published in the prestigious journal Molecular Psychiatry the pioneering study PREDICT-gene, confirming the relation between allele s in the serotonin transporter gene and exposure to threatening life events in the onset of depression. The study proves, for a population sample accounting for gender, age and family history of psychiatric disorders, that 24% of the Spanish population, comprising people with the s/s genotype, need minimal exposure to threatening life events, unlike individuals with s/l or l/l genotypes, thus confirming the relation between genetic and environmental factors in this mental disorder.

Tailor-made antidepressants

The most important consequence of research on interaction between genetic and environmental factors is that, in a foreseeable future, scientists will be able to produce measures to predict response to antidepressants taking into account each individual’s genotype, i. e. they will be able to design tailor-made drugs according to each person’s genetic configuration and their exposure to environmental factors.

The research group headed by professor Cervilla Ballesteros and Gutiérrez Martínez is currently working at the University of Granada to open roads for psycho-pharmaco-genetics, a field that will allow for individual treatments, tailor-made drugs, for each patient with depression, a disorder affecting one in every five Spaniards visiting the doctor’s.

This study is framed in the international project PREDICT and is funded by the European Union and the Spanish Ministry of Education and Science. One of its most important novelties is that it has been carried out through a very representative sample: a total of 737 people agreed to participate in the genetic tests, with ages ranging from 18 to 75, patients of nine primary care centres in the South of Spain. That is why this is the first representative population-based replication of earlier research, as until now research had been done into restricted population samples, comprising only women, adolescents, twins or people with affective disorders.

Contact: Professor Jorge Cervilla Ballesteros
jacb@ugr.es
34-663-075-835
Universidad de Granada

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August 6, 2007 Posted by | Alberta, Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Canada, Depression, France, General Psychiatry, Germany, Global, Global Health Vision, Global News, Health Canada, Music Video Pick Of The Day, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, Nova Scotia, Osaka, Ottawa, Prince Edward Island, Public Health, Quebec, RSS, RSS Feed, Spain, Toronto, UK, US, Virginia, Washington DC, Washington DC City Feed, World News | Leave a comment

European heat waves double in length since 1880

The most accurate measures of European daily temperatures ever indicate that the length of heat waves on the continent has doubled and the frequency of extremely hot days has nearly tripled in the past century. The new data shows that many previous assessments of daily summer temperature change underestimated heat wave events in western Europe by approximately 30 percent.

Paul Della-Marta and a team of researchers at the University of Bern in Switzerland compiled evidence from 54 high-quality recording locations from Sweden to Croatia and report that heat waves last an average of 3 days now—with some lasting up to 4.5 days—compared to an average of around 1.5 days in 1880. The results are published 3 August in the Journal of Geophysical Research-Atmospheres, a publication of the American Geophysical Union. The researchers suggest that their conclusions contribute to growing evidence that western Europe’s climate has become more extreme and confirm a previously hypothesized increase in the variance of daily summer temperatures since the 19th century.

The study adds evidence that heat waves, such as the devastating 2003 event in western Europe, are a likely sign of global warming; one that perhaps began as early as the 1950s, when their study showed some of the highest trends in summer mean temperature and summer temperature variance.

“These results add more evidence to the belief among climate scientists that western Europe will experience some of the highest environmental and social impacts of climate change and continue to experience devastating hot summers like the summer of 2003 more frequently in the future,” Della-Marta said.

The authors note that temperature records were likely overestimated in the past, when thermometers were not kept in modern Stevenson screens, which are instrument shelters used to protect temperature sensors from outside influences that could alter its readings. The researchers corrected for this warm bias and other biases in the variability of daily summer temperatures and show that nearly 40 percent of the changes in the frequency of hot days are likely to be caused by increases in summer temperatures’ variability. This finding demonstrates that even a small change in the variance of daily summer temperatures can radically enhance the number of extremely hot days.

“These findings provide observational support to climate modeling studies showing that European summer temperatures are particularly sensitive to global warming,” Della-Marta said. “Due to complex reactions between the summer atmosphere and the land, the variability of summer temperatures is expected to [continue to] increase substantially by 2100.”

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The research was supported by the European Environment and Sustainable Development Program, the Swiss National Science Foundation and the National Center for Excellence in Climate Research (NCCR Climate).

Contact: Jonathan Lifland
jlifland@agu.org
202-777-7535
American Geophysical Union

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August 3, 2007 Posted by | Alberta, Baltimore, Barcelona, Bethesda, Calgary, Canada, France, Germany, Global, Global Health Vision, Global News, Health Canada, Irvine, Italy, Japan, Medical Journals, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, Nova Scotia, Osaka, Ottawa, Pennsylvania, Prince Edward Island, Quebec, RSS, RSS Feed, Slovakia, Spain, Toronto, UK, University of Bern, US, Virginia, Washington DC, Washington DC City Feed | Leave a comment

U-M researchers find family of ‘on switches’ that cause prostate cancer

Gene fusions trigger cancer growth, could impact treatment choices

ANN ARBOR, Mich. — Researchers at the University of Michigan Comprehensive Cancer Center have discovered how genes turn on the switch that leads to prostate cancer.

The team discovered that pieces of two chromosomes can trade places with each other and cause two genes to fuse together. The fused genes then override the “off” switch that keeps cells from growing uncontrollably, causing prostate cancer to develop.

By testing these gene fusions in mice and in cell cultures, the researchers showed that the fusions are what cause prostate cancer to develop. But it’s not just one set of genes that fuse. The researchers found that any one of several in a family of genes can become scrambled and fuse. Results of the study appear in the Aug. 2 issue of Nature.

“Each of these switches, or gene fusions, represent different molecular subtypes. This tells us there’s not just one type of prostate cancer. It’s a more complex disease and potentially needs to be treated differently in each patient,” says lead study author Arul Chinnaiyan, M.D., Ph.D., director of the Michigan Center for Translational Pathology, a new U-M center whose goal is to translate research into real world practice.

The gene fusion research is the centerpiece project of the new center. In the current study, researchers found one of several abnormal gene fusions in the prostate cancer tissue samples they tested. In 2005, the researchers identified a prostate-specific gene called TMPRSS2, which fuses with either ERG or ETV1, two genes known to be involved in several types of cancer.

The Nature paper reports on five additional genes that fuse with ERG or ETV1 to cause prostate cancer. Gene fusions were involved in 60 percent to 70 percent of the prostate cancer cell lines the researchers looked at. The genes involved are all controlled by a different mechanism. For example, four of the genes are regulated by androgen, a male sex hormone known to fuel prostate cancer. Androgen deprivation is a common therapy for prostate cancer.

Knowing which gene fusion is involved in an individual patient’s tumor could impact treatment options. If an androgen-regulated gene is involved, androgen therapy would be appropriate. But if the gene fusion involves a gene that represses androgen, the anti-androgen therapy could encourage the cancer’s growth. This may also explain why androgen treatment is not effective for some prostate cancers.

“Typing someone’s prostate cancer by gene fusion can affect the treatment given. We would not want to give androgen to someone whose prostate cancer gene fusion is not regulated by androgen,” says Chinnaiyan, who is the S.P. Hicks Collegiate Professor of Pathology at the U-M Medical School.

Rearrangements in chromosomes and fused genes are known to play a role in blood cell cancers like leukemia and lymphoma, and in Ewing’s sarcoma. A fused gene combination that plays a role in chronic myelogenous leukemia led researchers to develop the drug Gleevec, which has dramatically improved survival rates for that disease.

Chinnaiyan believes the prostate gene fusions will eventually lead to similar treatments for prostate cancer.

“More immediately, we hope to develop tests for diagnosis or prognosis. But long-term, we hope this will lead to better therapies to treat prostate cancer. The key challenge is to find a drug that would go after this gene fusion,” Chinnaiyan says.

The gene fusion technology has been licensed to San Diego-based Gen-Probe Inc., which is working on a screening tool to detect gene fusions in urine. The tool could one day supplement or replace the prostate specific antigen, or PSA, test currently used to screen for prostate cancer.

The idea of translating laboratory research findings into a test or treatment that will impact patients is central to the new Michigan Center for Translational Pathology. The center brings together experts in genomics, proteomics and bioinformatics to look at common patterns and potential targets in cancer and other diseases. This is the first center of its kind in the nation in that it is associated with one of 39 National Cancer Institute-designated “comprehensive” cancer centers, a premier medical school and a large health system with both clinicians and patients.

The center’s goal is to study the genes, proteins and other markers on cells to develop new diagnostic tests or screening tools as well as targeted treatments for cancer and other diseases, with the key being to translate these laboratory discoveries into clinical applications.

Chinnaiyan and his team have received numerous awards and honors, including the American Association for Cancer Research Team Science Award for their previously published work on gene fusions, and the Specialized Program of Research Excellence Outstanding Investigator award. The new Center for Translational Pathology supported in part by the Prostate Cancer Foundation, which has offered to match up to $1 million dollars in donations to support work related to developing therapies against prostate cancer gene fusions at the university.

“Mapping of the human genome was only the beginning. Equipped with the comprehensive analysis of the human genome, we can now systematically examine the blueprint of disease at the molecular level. This essential knowledge may lead to better diagnostic tests and promising new treatments for cancer, cardiovascular disease, diabetes and other illnesses,” Chinnaiyan says.

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For information about the Michigan Center for Translational Pathology, go to http://www.med.umich.edu/mctp.

About 218,890 men will be diagnosed with prostate cancer this year, and 27,050 will die from the disease, according to the American Cancer Society. The gene fusion work is not currently available for treatment or diagnosis, and no clinical trials are currently recruiting. For information about prostate cancer and currently available treatments, go to http://www.mcancer.org or call the U-M Cancer AnswerLine at 800-865-1125.

In addition to Chinnaiyan, U-M study authors were Scott Tomlins; Saravana Dhanasekaran, Ph.D.; Bharathi Laxman; Qi Cao; Beth Helgeson; Xuhong Cao; David Morris, M.D.; Anjana Menon; Xiaojun Jing; Bo Han; James Montie, M.D.; Kenneth Pienta, M.D.; Diane Roulston; Rajal Shah, M.D.; Sooryanarayana Varambally, Ph.D.; and Rohit Mehra, M.D. Mark Rubin, M.D., from Brigham and Women’s Hospital, Dana-Farber Cancer Institute and Harvard Medical School is also a study author.

Funding for the study came from the U.S. Department of Defense, the National Institutes of Health, the Early Detection Research Network, the Prostate Cancer Foundation and Gen-Probe Inc.

The University of Michigan has filed for a patent on the detection of gene fusions in prostate cancer, on which Tomlins, Mehra, Rubin and Chinnaiyan are co-inventors. The diagnostic field of use has been licensed to Gen-Probe Inc. Chinnaiyan also has a sponsored research agreement with Gen-Probe; however, GenProbe has had no role in the design or experimentation of this study, nor has it participated in the writing of the manuscript.

Reference: Nature, Vol. 448, No. 7153, Aug. 2, 2007

Contact: Nicole Fawcett
nfawcett@umich.edu
734-764-2220
University of Michigan Health System

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Huntington’s disease study shows animal models on target

This release is available in French.

An international team of researchers has published a benchmark study showing that gene expression in several animal models of Huntington’s Disease (HD) closely resembles that of human HD patients.

The results, published August 1, 2007, in the , validate the applicability of using animal models to study human disease and will have important consequences for the pertinence of these models in preclinical drug testing.

Huntington’s disease is an incurable and fatal hereditary neurodegenerative disorder caused by a mutation in the gene that encodes the huntingtin protein. Neurons in certain regions of the brain succumb to the effects of the altered protein, leading to severe motor, psychiatric, and cognitive decline. Several recent studies have shown that the mutant huntingtin protein modifies the transcriptional activity of genes in affected neurons. This disease mechanism is a promising new avenue for research into the causes of neuronal death and a novel potential approach for treatment.

Led by EPFL professor Ruth Luthi-Carter, and involving collaborators from six countries, the current study found a marked resemblance between the molecular etiology of neurons in animal models and neurons in patients with HD. This implies that animal models are relevant for studying human HD and testing potential treatments.

To come to this conclusion, the scientists measured the gene expression profile of seven different transgenic mouse models of HD, representing different conditions and disease stages. These profiles clarified the role of different forms and dosages of the protein hungtintin in the transcriptional activity of neurons. They then designed and implemented novel computational methods for quantifying similarities between RNA profiles that would allow for comparisons between the gene expression in mice and in human patients. “Interestingly, results of different testing strategies converged to show that several available models accurately recapitulate the molecular changes observed in human HD,” explains Luthi-Carter. “It underlines the suitability of these animal models for preclinical testing of drugs that affect gene transcription in Huntington’s Disease.”

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More Information:

EPFL Laboratory of functional neurogenomics, http://lngf.epfl.ch/

Alexandre Kuhn ; +41 21 693 1731
alexandre.kuhn@epfl.ch

Professor Ruth Luthi-Carter; +41 21 693 9533
ruth.luthi-carter@epfl.ch

Contact: Alexandre Kuhn
alexandre.kuhn@epfl.ch
41-216-931-731
Ecole Polytechnique Fédérale de Lausanne

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Flip of genetic switch causes cancers in mice to self-destruct, Stanford researchers find

STANFORD, Calif. – Killing cancerous tumors isn’t easy, as anyone who has suffered through chemotherapy can attest. But a new study in mice shows that switching off a single malfunctioning gene can halt the limitless division of tumor cells and turn them back to the path of their own planned obsolescence.

The surprising possibility that a cell’s own natural mechanism for ensuring its mortality could be used to vanquish tumors opens the door to a new approach to developing drugs to treat cancer patients, according to Dean Felsher, MD, PhD, associate professor of medicine (oncology) and of pathology at the Stanford University School of Medicine. Felsher is the senior author of the study to be published July 30 in the advance online version of the Proceedings of the National Academy of Sciences.

“Our research implies that by shutting off a critical cancer gene, tumor cells can realize that they are broken and restore this physiologic fail-safe program,” said Felsher.

Cancer can be notoriously resistant to medical treatment. Not only do cancer cells proliferate uncontrollably, they somehow circumvent the mechanism that causes normal cells to die when they get old or malfunction. That makes cancer cells effectively immortal unless doctors manage to squelch them.

The gene Felsher’s team studied produces a protein called Myc (pronounced “mick”), which promotes cell division. A mutation of the gene causes cells to overproduce the protein, prompting perpetual cell division and tumor growth. By turning off the mutated gene, the researchers found that not only did uncontrolled cell division cease, but the cells also reactivated a normal physiological mechanism, called senescence, which makes it possible for a cell to eventually die.

“What was unexpected was just the fact that cancer cells had retained the ability to undergo senescence at all,” said Felsher. Cancer researchers had long thought the senescence process had to be irreversibly disrupted for a tumor to develop.

The researchers worked with a series of mice engineered to have Myc-triggered cancers of either the liver, blood or bones, along with a specially constructed version of the Myc gene that they could switch off by feeding the mice antibiotics. When the mice dined on doses of the drugs, invariably, the tumors ceased growing and then diminished, with some disappearing over the course of just a few days.

Although Felsher’s lab had previously shown that mouse tumors diminished and disappeared when Myc was switched off, they hadn’t been sure how the process actually worked. Historically, most research involving genetic methods of battling cancer cells has focused on reactivating genes called tumor-suppressor genes, which are generally overcome by a proliferating cancer. No one had explored the idea that senescence might play a key role in diminishing tumors.

Felsher described senescence as acting like a fail-safe mechanism to stop cancer. When a cell detects a deleterious mutation, it launches the senescence process, resulting in the permanent loss of the cell’s ability to proliferate, thus halting any cancer.

“In order to become tumor cells, those cells have to overcome senescence,” said Chi-Hwa Wu, PhD, postdoctoral researcher in Felsher’s lab and first author of the study. Wu had the inspiration to explore whether the sudden diminishment they had observed in the tumors might be due to the reactivation of some latent remnant of the trigger for senescence.

Through a series of experiments looking at enzymes associated with the senescence process, as well as some molecular markers, Wu confirmed her suspicion. And not only was senescence occurring in cells that had been thought to be incapable of it, the process was reactivated in all the different tumors they studied.

Consider it a cell version of the Jekyll-and-Hyde transformation. “It’s sort of like Mr. Hyde realizing that there’s something wrong with him and then being able to put himself back into his normal state as Dr. Jekyll,” Felsher said.

In addition to the deepened understanding of how the process of senescence works, Felsher and Wu see a lot of potential for new approaches to treating cancer, beyond the traditional tactic of trying to kill cancer cells directly. “This work implies that maybe part of the strategy should involve figuring out how to get the cancer cells to just be allowed to do what they originally wanted to do anyway, which is to not be proliferating endlessly and growing uncontrolled,” said Felsher.

The next step for the team is to see how well the approach works in human cancer cells. “And we’re also trying to figure out what the mechanism is,” Felsher said. “What are the molecular mechanisms of this, so that we can figure out how to better treat cancer””

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Other authors on the research paper are Jan van Riggelen, PhD, postdoctoral researcher; Alper Yetil, graduate student in cancer biology; Alice Fan, MD, instructor in medicine (oncology), and medical student Pavan Bachireddy.

The study was funded by the National Cancer Institute, the National Institutes of Health, the Leukemia and Lymphoma Society, the Burroughs Wellcome Fund, the Damon Runyon Lilly Clinical Investigator Award, the Lymphoma Research Foundation and the Howard Hughes Medical Institute.

Stanford University Medical Center integrates research, medical education and patient care at its three institutions – Stanford University School of Medicine, Stanford Hospital & Clinics and Lucile Packard Children’s Hospital at Stanford. For more information, please visit the Web site of the medical center’s Office of Communication & Public Affairs at http://mednews.stanford.edu.

Contact: Lou Bergeron
louisb3@stanford.edu
650-723-3900
Stanford University Medical Center

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