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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

Political decisions harming cancer treatment in Europe

Time to stand up and be counted, say oncologists

Barcelona, Spain: Recent political decisions have had serious consequences for European oncology, said Professor John Smyth at ECCO 14, the European Cancer Conference, today (Monday 24 September 2007). Professor Smyth, President of the Federation of European Cancer Societies (FECS) said that the new European CanCer Organisation (ECCO) would take an active role in engaging with policymakers to ensure that future legislation did not have a similarly negative impact.

Professor Smyth cited the Clinical Trials Directive and the recent Directive on Physical Agents (Electromagnetic Fields) as two examples of legislation that had had a major negative impact on oncology in Europe. “In the first, the academic oncology community woke up too late and found that the administrative and financial burden of running clinical trials had increased to the extent that many simply gave up,” he said. “Now the Directive on Electromagnetic Fields looks as though it may stop all MRI scanning in Europe. We simply cannot continue to bury our heads in the sand on these issues, which affect doctors and patients alike.”

Forthcoming topics of concern were the problems of international collaboration on stem cell research where European countries had widely differing legislation, and the whole area of the escalating cost of cancer treatment. “The successful development of many new anti-cancer drugs in recent years is challenging every health economic programme in Europe,” said Professor Smyth. “It is imperative to find ways to improve the cost effectiveness of cancer treatment in general, and particularly the use of drugs. Improving the cost effective use of medicines is a major priority for industry, politicians and the public at large.

“Due to these new and improved treatments, screening, and earlier and better diagnosis, cancer patients are living longer and better lives. But how will the huge financial burden on society that this implies be met” ECCO will be asking governments and the European Commission to consider these issues as a matter or urgency.”

ECCO will bring together major players in cancer research, treatment, and care in order to create awareness of patients’ wishes and needs, encourage progressive thinking in cancer policy, education, and training, and continue to promote European cancer research and its application through the organisation of multi-disciplinary meetings and conferences, he said.

“The difference between the new ECCO and the old FECS will be that the new organisation has decided to take a far more active role in engaging with policymakers to promote the interests of both cancer patients, those who care for them; and those without whose research there would be no advances in treatment and care,” he said. “For too long oncologists have sat back and said that getting involved in politics is not their business, and recent events have shown us that this is an attitude which is no longer sustainable.”

The last two years had given ample opportunity for reflection, said Professor Smyth. “Not only did we consult our members, but we also carried out an audit of many players in oncology, patient groups, media, and other stakeholders. They all told us the same thing – they wanted to see a democratic, representative, and visionary organisation tackle the problems that are currently besetting oncology science and practice. An organisation that would provide consistently dependable information on the state of oncology in Europe, and through that information provision would strive to improve the lot of everyone involved in cancer.

“It is a daunting task, but one that needs to be undertaken. And we will do our very best to carry it out.”

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Notes for Editors:

1. Invitations to join ECCO (http://www.ecco-org.eu/) have been sent to the FECS Founding Members: EACR, EONS, ESSO, ESMO, ESTRO, and SIOP Europe.
Members and Advisory Council: EANO, EORTC, ESGO, ESO, ESOP, Euroskin, and EUSOMA, EBMT, ECL, Europa Donna, FAC, OECI, and UICC.

2. The Clinical Trials Directive 2001/20/EC came into force in 2004. Its aim was to harmonise national legislation on the conduct of clinical trials and to create a level playing field for European clinical research. In fact it seems to have had the opposite effect, with academic researchers finding that the extra administrative and financial burden that it imposes impedes severely their chances of carrying independent, objective research.

3. The Physical Agents (Electromagnetic Fields) Directive 2004/40/EC is intended to protect workers from electromagnetic radiation. However, its implementation in its current form would effectively ban all MRI scanning in Europe, since the limits it sets to occupational radiation exposure would mean that anyone working or moving near MRI equipment will breach them, thus making it possible for them to sue their employers.

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September 24, 2007 Posted by | Cancer, European Cancer Conference, Global Health Vision, Global News, News, News UK | 2 Comments

Embryonic stem cells used to grow cartilage

Rice method is first to yield cartilage-like cells, engineer human cartilage

HOUSTON, Sept. 6, 2007 – Rice University biomedical engineers have developed a new technique for growing cartilage from human embryonic stem cells, a method that could be used to grow replacement cartilage for the surgical repair of knee, jaw, hip, and other joints.

“Because native cartilage is unable to heal itself, researchers have long looked for ways to grow replacement cartilage in the lab that could be used to surgically repair injuries,” said lead researcher Kyriacos A. Athanasiou, the Karl F. Hasselmann Professor of Bioengineering. “This research offers a novel approach for producing cartilage-like cells from embryonic stem cells, and it also presents the first method to use such cells to engineer cartilage tissue with significant functional properties.”

The results are available online and slated to appear in the September issue of the journal Stem Cells. The study involved cells from an NIH-sanctioned stem cell line.

Using a series of stimuli, the researchers developed a method of converting the stem cells into cartilage cells. Building upon this work, the researchers then developed a process for using the cartilage cells to make cartilage tissue. The results show that cartilages can be generated that mimic the different types of cartilage found in the human body, such as hyaline articular cartilage — the type of cartilage found in all joints — and fibrocartilage — a type found in the knee meniscus and the jaw joint. Athanasiou said the results are exciting, as they suggest that similar methods may be used to convert the stem cell-derived cartilage cells into robust cartilage sections that can be of clinical usefulness.

Tissue engineers, like those in Athanasiou’s research group, are attempting to unlock the secrets of the human body’s regenerative system to find new ways of growing replacement tissues like muscle, skin, bone and cartilage. Athanasiou’s Musculoskeletal Bioengineering Laboratory at Rice University specializes in growing cartilage tissues.

The idea behind using stem cells for tissue engineering is that these primordial cells have the ability to become more than one type of cell. In all people, there are many types of “adult” stem cells at work. Adult stem cells can replace the blood, bone, skin and other tissues in the body. Stem cells become specific cells based upon a complex series of chemical and biomechanical cues, signals that scientists are just now starting to understand.

Unlike adult stem cells, which can become only a limited number of cell types, embryonic stem cells can theoretically become any type of cell in the human body.

Athanasiou’s group has been one of the most successful in the world at studying cartilage cells and, especially, engineering cartilage tissues. He said that for his research the primary advantage that embryonic stem cells have over adult stem cells is their ability to remain malleable.

“Identifying a readily available cell source has been a major obstacle in cartilage engineering,” Athanasiou said. “We know how to convert adult stem cells into cartilage-like cells. The more problematic issue comes in trying to maintain a ready stock of adult stem cells to work with. These cells have a strong tendency to convert from stem cells into a more specific type of cell, so the clock is always ticking when we work with them.”

By contrast, Athanasiou said his research group has found it easier to grow and maintain a stock of embryonic stem cells. Nonetheless, he is quick to point out that there is no clear choice about which type of stem cell works best for cartilage engineering.

“We don’t know the answer to that,” Athanasiou said. “It’s extremely important that we study all potential cell candidates, and then compare and contrast those studies to find out which works best and under what conditions. Keep in mind that these processes are very complicated, so it may well be that different types of cells work best in different situations.”

Athanasiou began studying embryonic stem cells in 2005. Since funding for the program was limited, he asked two new graduate students in his group if they were interested in pursuing the work as a secondary project to their primary research. Those students, Eugene Koay and Gwen Hoben, are co-authors of the newly published study. Both are enrolled in the Baylor College of Medicine Medical Scientist Training Program, a joint program that allows students to concurrently earn their medical degree from Baylor while undertaking Ph.D. studies at Rice.

“Eugene and Gwen are both outstanding students,” Athanasiou said. “Each earned their undergraduate degree from Rice and each worked in my laboratory as undergraduate students. They have chosen to do this research because they think this may represent the future of regenerative medicine.”

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The research was funded by Rice University.

Contact: Jade Boyd
jadeboyd@rice.edu
713-348-6778
Rice University

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September 7, 2007 Posted by | Global Health Vision, Global News, Health, Health Canada, HIV, Hospital Epidemiology, News UK, News USA, RSS, Science, Stem Cells | Leave a comment

Can cancer drugs combine forces?

Individuals with chronic myeloid leukemia (CML) are treated first with a drug known as imatinib (Gleevec), which targets the protein known to cause the cancer (BCR-ABL). If their disease returns, because BCR-ABL mutants emerge that are resistant to the effects of imatinib, individuals are treated with a drug known as dasatinib (SPRYCEL), which targets BCR-ABL in a different way. However, patients that relapse after treatment with dasatinib, because BCR-ABL mutants emerge that are resistant to the effects of this drug, are now beginning to be seen in the clinic. Researchers from Memorial Sloan-Kettering Cancer Center, New York, now suggest that treating patients with a combination of the drugs might decrease the chance of the cancer returning, or at the very least increase the time before a relapse occurs

In the study, which appears online on August 16 in advance of publication in the September print issue of the Journal of Clinical Investigation, Charles Sawyers and colleagues show that 2 of 12 patients whose cancer had returned after treatment with dasatinib responded to retreatment with imatinib. Analysis of the BCR-ABL proteins from these patients revealed that their BCR-ABL had only the dasatinib-resistance mutation. By contrast, the BCR-ABL proteins of the other patients had either a single mutation that rendered the protein resistant to both dasatinib and imatinib or had two mutations, one rendering the protein resistant to imatinib and one rendering the protein resistant to dasatinib. A third drug that can target dasatinib- and imatinib-resitant BCR-ABL is currently in clinical trials. The authors therefore suggest that rather than treating CML patients with the drugs that target BCR-ABL sequentially, they should receive all the drugs when they are first diagnosed with the disease so that the emergence of the drug-resistant forms of BCR-ABL might be prevented, or at least delayed.

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TITLE: Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency

AUTHOR CONTACT: Charles L. Sawyers Memorial Sloan-Kettering Cancer Center, New York, New York, USA. Phone: (646) 888-2138; Fax: (646) 888-2595; E-mail: sawyersc@mskcc.org.

View the PDF of this article at: https://www.the-jci.org/article.php?id=30890

Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation

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August 16, 2007 Posted by | Cancer, Global Health Vision, Global News, Health, Leukemia, News UK, News USA | 1 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

Multicenter study nets new lung tumor-suppressor gene

BOSTON–Collaborating scientists in Boston and North Carolina have found that a particular gene can block key steps of the lung cancer process in mice. The researchers report in the journal Nature that LKB1 is not only a “tumor-suppressor” gene for non-small cell lung cancer in mice, it also may be more powerful than other, better-known suppressors. The study will be published on the journal’s Web site on Aug. 5 and later in a print version.

If further research shows LKB1 has a similar effect in human lung cells, it could influence the way non-small cell lung cancer is diagnosed and treated, says the study’s senior author, Kwok-Kin Wong, MD, PhD, of Dana-Farber, one of three institutions, along with Massachusetts General Hospital and the University of North Carolina School of Medicine, leading the work. If tumors with LKB1 mutations are found to be especially fast-growing, for example, patients with such tumors might be candidates for more aggressive therapy.

People born with defective versions of LKB1 often develop Peutz-Jeghers syndrome, which is marked by intestinal growths and an increased risk for certain cancers. Non-inherited mutations of the gene have been found in some lung cancers. This suggested that LKB1 normally thwarts tumors from forming. Mutated versions may be unable to act as a brake on cancer.

To find out, the investigators ran a series of experiments in mice with a defective form of a gene called Kras, which drives the formation and growth of lung cancer. They tracked the development of lung cancer in animals with mutated LKB1 and compared it to the experience of animals with abnormalities in either of two well-known tumor-suppressor genes.

They found that while Kras “cooperated” with the mutated tumor-suppressor genes to produce lung cancer, it cooperated even more strongly with mutated LKB1. “The LKB1-deficient tumors grew more rapidly and spread more frequently than the others, and comprised all three types of non-small cell lung cancer — squamous cell carcinoma, large-cell carcinoma, and adenocarcinoma — rather than just one or two,” Wong says. “This suggests that LKB1 plays a role at major stages of the tumors’ development: initiation, differentiation of normal lung cells into cancer cells, and metastasis.”

An examination of human non-small-cell lung tissue suggests LKB1 mutations play a role there as well. Of 144 samples analyzed, 34 percent of the lung adenocarcinomas and 19 percent of the squamous cell carcinomas contained abnormal versions of the gene, researchers report.

“We were surprised at how significant a role LKB1 mutations play in non-small cell lung cancer development in mice,” say Wong, who is also an assistant professor of medicine at Harvard Medical School. “This suggests there may be additional lung tumor-suppressor genes yet to be discovered. We’re currently examining whether these results apply to human lung cancers as well and, if so, how such information can improve treatment.”

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The lead author of the study was Hongbin Ji, PhD, of Dana-Farber. Other Dana-Farber co-authors include Dongpo Cai, PhD, Liang Chen, PhD, Pasi Janne, MD, PhD, Bruce Johnson, MD, Jussi Koivunen, MD, PhD, Danan Li, Mei-Chih Liang, PhD, Kate McNamara, Matthew Meyerson, MD, PhD, Samanthi Perera, PhD, Geoffrey Shapiro, MD, PhD, and Takeshi Shimamura, PhD. Other authors were based at Children’s Hospital Boston, Brigham and Women’s Hospital, Broad Institute of Harvard University and Massachusetts Institute of Technology, University of Tennessee Health Science Center, and the University of Texas Southwestern Medical Center.

The research was supported by the National Institutes of Health, the Sidney Kimmel Foundation for Cancer Research, the American Federation of Aging, the Joan Scarangello Foundation to Conquer Lung Cancer, the Flight Attendant Medical Research Institute, the Waxman Foundation, the Harvard Stem Cell Institute, and the Linda Verville Foundation.

Dana-Farber Cancer Institute (www.dana-farber.org) is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute.

Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute

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August 5, 2007 Posted by | Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Canada, Cancer, Cancer Biology, France, Genes, Genetic, Genetic Link, Genetics, Genome, Genomic, Germany, Global, Global Health Vision, Global News, Health Canada, Human Genome, LKB1, Lung Cancer, Medical History, Medical Journals, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, NIH, Peutz-Jeghers syndrome, University of North Carolina, World News | 2 Comments

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

Identifying the mechanism behind a genetic susceptibility to type 2 diabetes

Type 2 diabetes is reaching epidemic proportions in the developed world. Determining if and how certain genes predispose individuals to type 2 diabetes is likely to lead to the development of new treatment strategies for individuals with the disease.

In a study appearing in the August issue of the Journal of Clinical Investigation Valeriya Lyssenko and colleagues from Lund University in Sweden show that certain variants of the gene TCF7L2 make individuals more susceptible to type 2 diabetes. The susceptibility variants were associated with increased expression of TCF7L2 in pancreatic islet cells and decreased islet cell secretion of insulin. Consistent with this, ectopic overexpression of TCF7L2 in human islet cells decreased insulin secretion in response to exposure to glucose. This study identifies TCF7L2 type 2 diabetes susceptibility variants and provides a mechanism by which these genetic variants might cause susceptibility to the disease. As discussed by the authors and in the accompanying commentary by Andrew Hattersley from Peninsula Medical School in the United Kingdom, future studies are likely to investigate the potential for manipulating the signaling pathways controlled by TCF7L2 for the development of new therapeutics for type 2 diabetes.

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TITLE: Mechanisms by which common variants in the TCF7L2 gene increase risk of type 2 diabetes

AUTHOR CONTACT:
Valeriya Lyssenko
Lund University, University Hospital Malma, Malma, Sweden.
Phone: 46-40-391214; Fax: 46-40-391222; E-mail: Valeri.Lyssenko@med.lu.se.

View the PDF of this article at: https://www.the-jci.org/article.php?id=30706

ACCOMPANYING COMMENTARY
TITLE: Prime suspect: the TCF7L2 gene and type 2 diabetes risk

AUTHOR CONTACT:
Andrew T. Hattersley
Institute of Biomedical and Clinical Sciences, Peninsula Medical School, Exeter, United Kingdom.
Phone: 44-1392-406806; Fax: 44-1392-406767; E-mail: Andrew.Hattersley@pms.ac.uk.

View the PDF of this article at: https://www.the-jci.org/article.php?id=33077

Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation

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August 2, 2007 Posted by | Alberta, Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Canada, Diabetes, France, Genes, Genetic, Genetic Link, Genetics, Genome, Genomic, Germany, Global, Global Health Vision, Global News, Health Canada, Human Genome, Irvine, Italy, Japan, Journal of Clinical Investigation, Medical Journals, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, Nova Scotia, Nunavut, Osaka, Ottawa, Pennsylvania, Prince Edward Island, Public Health, Quebec, Research, RSS, RSS Feed, Slovakia, Spain, Toronto, Type 2 Diabetes, US, Virginia, Washington DC, Washington DC City Feed, World News | 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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