Doctors to vote on cigarette sale ban for those born after 2000 .


One of the deadliest forms of paediatric brain tumour, Group 3 medulloblastoma, is linked to a variety of large-scale DNA rearrangements which all have the same overall effect on specific genes located on different chromosomes. The finding, by scientists at the European Molecular Biology Laboratory (EMBL), the German Cancer Research Centre (DKFZ), both in Heidelberg, Germany, and Sanford-Burnham Medical Research Institute in San Diego, USA, is published online today in Nature.

Teenage girls smoking

To date, the only gene known to play an important role in Group 3 medulloblastoma was a gene called MYC, but that gene alone couldn’t explain some of the unique characteristics of this particular type of medulloblastoma, which has a higher metastasis rate and overall poorer prognosis than other types of this childhood . To tackle the question, Jan Korbel’s group at EMBL and collaborators at DKFZ tried to identify new involved, taking advantage of the large number of medulloblastoma genome sequences now known.

“We were surprised to see that in addition to MYC there are two other major drivers of Group 3 medulloblastoma – two sister genes called GFI1B and GFI1,” says Korbel. “Our findings could be relevant for research on other cancers, as we discovered that those genes had been activated in a way that cancer researchers don’t usually look for in solid tumours.”

Rather than take the usual approach of looking for changes in individual genes, the team focused on large-scale rearrangements of the stretches of DNA that lie between genes. They found that the DNA of different patients showed evidence of different rearrangements: duplications, deletions, inversions, and even complex alterations involving many ‘DNA-shuffling’ events. This wide array of genetic changes had one effect in common: they placed GFI1B close to highly active enhancers – stretches of DNA that can dramatically increase gene activity. So large-scale DNA changes relocate GFI1B, activating this gene in cells where it would normally be switched off. And that, the researchers surmise, is what drives the tumour to form.

“Nobody has seen such a process in solid cancers before,” says Paul Northcott from DKFZ, “although it shares similarities with a phenomenon implicated in leukaemias, which has been known since the 80s.”

GFI1B wasn’t affected in all cases studied, but in many patients where it wasn’t, a related gene with a similar role, GFI1, was. GFI1B and GFI1 sit on different chromosomes, and interestingly, the DNA rearrangements affecting GFI1 put it next to enhancers sitting on yet other chromosomes. But the overall result was identical: the gene was activated, and appeared to drive tumour formation.

To confirm the role of GFI1B and GFI1 in causing medulloblastoma, the Heidelberg researchers turned to the expertise of Robert Wechsler-Reya’s group at Sanford-Burnham. Wechsler-Reya’s lab genetically modified to have either GFI1B or GFI1 turned on, together with MYC. When they inserted those modified cells into the brains of healthy mice, the rodents developed aggressive, metastasising brain tumours that closely resemble Group 3 medulloblastoma in humans.

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These mice are the first to truly mimic the genetics of the human version of Group 3 medulloblastoma, and researchers can now use them to probe further. The mice could, for instance, be used to test potential treatments suggested by these findings. One interesting option to explore, the scientists say, is that highly active enhancers – like the ones they found were involved in this tumour – can be vulnerable to an existing class of drugs called bromodomain inhibitors. And, since neither GFI1B nor GFI1 is normally active in the brain, the study points to possible routes for diagnosing this brain tumour, too.

But the mice also raised another question the scientists are still untangling. For the rodents to develop -like tumours, activating GFI1 or GFI1B was not enough; MYC also had to be switched on. In human patients, however, scientists have found a statistical link between MYC and GFI1, but not between MYC and GFI1B, so the team is now following up on this partial surprise.

“What we’re learning from this study is that clearly one has to think outside the box when trying to understand cancer genomes,” Korbel concludes.

Overlooked DNA shuffling drives deadly paediatric brain tumour


Melbourne researchers have shown a type of leukemia can be successfully ‘reversed’ by coaxing the cancer cells back into normal development. The discovery was made using a model of B-progenitor acute lymphoblastic leukemia (B-ALL), the most common cancer affecting children. Researchers from the Walter and Eliza Hall Institute showed that switching off a gene called Pax5 could cause cancer in a model of B-ALL, while restoring its function could ‘cure’ the disease.

Institute researchers Dr Ross Dickins and Ms Grace Liu led the study with institute colleagues and collaborators in Vienna. The study was published in the journal Genes & Development.

Ms Liu said the team used a newly developed ‘genetic switch’ technology to inhibit then reactivate Pax5 in the leukemia model.

“Along with other genetic changes, deactivating Pax5 drives normal blood cells to turn into leukemia cells, which has been shown before,” Ms Liu said. “However we showed for the first time that reactivating Pax5 enabled the cells to resume their normal development and lose their cancer-like qualities, effectively curing the leukemia. What was intriguing for us was that simply restoring Pax5 was enough to normalize these cancer cells, despite the other genetic changes.”

In leukemia, immature white blood cells replicate abnormally and build up in the bone marrow, interfering with production of normal blood cells.

Ms Liu said Pax5 was a gene frequently ‘lost’ in childhood B-ALL. “Pax5 is essential for normal development of a type of white blood cells called B cells,” she said. “When Pax5 function is compromised, developing B cells can get trapped in an immature state and become cancerous. We have shown that restoring Pax5 function, even in cells that have already become cancerous, removes this ‘block’, and enables the cells to develop into normal white blood cells.”

Dr Dickins said the research shed light on the function of Pax5, which was one of about 100 genes known to ‘suppress’ human tumors. “When these tumor suppressor genes are inactivated by changes to the DNA, cancers start to develop,” Dr Dickins said.

“This work shows how inactivating the tumor suppressor gene Pax5 contributes to B-ALL development and how leukemia cells become ‘addicted’ to low Pax5 levels to continue proliferating. Even though the B-ALL cells have multiple genetic mutations, simply reactivating Pax5 causes tumor cells to resume normal development and lose their cancerous properties.”

Dr Dickins said forcing B-ALL cells to resume their normal development could provide a new strategy for treating leukemia. “While B-ALL has a relatively good prognosis compared with other cancers, current treatments can last years and have major side-effects. By understanding how specific genetic changes drive B-ALL, it may be possible to develop more specific treatments that act faster with fewer side-effects.”

However Dr Dickins said that genes that are lost in tumor cells are not traditionally drug targets. “It is very difficult to develop drugs that restore the function of genes that are lost during cancer development,” Dr Dickins said. “However by understanding the mechanisms by which Pax5 loss causes leukemia, we can begin to look at ways of developing drugs that could have the same effect as restoring Pax5 function.”

The genetic switch technology used to study Pax5 could also be used to understand ‘tumour suppressor’ genes in other cancers, he said.

Gene ‘Switch’ Reverses Cancer in Common Childhood Leukemia Model


Melbourne researchers have shown a type of leukemia can be successfully ‘reversed’ by coaxing the cancer cells back into normal development. The discovery was made using a model of B-progenitor acute lymphoblastic leukemia (B-ALL), the most common cancer affecting children. Researchers from the Walter and Eliza Hall Institute showed that switching off a gene called Pax5 could cause cancer in a model of B-ALL, while restoring its function could ‘cure’ the disease.

Institute researchers Dr Ross Dickins and Ms Grace Liu led the study with institute colleagues and collaborators in Vienna. The study was published in the journal Genes & Development.

Ms Liu said the team used a newly developed ‘genetic switch’ technology to inhibit then reactivate Pax5 in the leukemia model.

“Along with other genetic changes, deactivating Pax5 drives normal blood cells to turn into leukemia cells, which has been shown before,” Ms Liu said. “However we showed for the first time that reactivating Pax5 enabled the cells to resume their normal development and lose their cancer-like qualities, effectively curing the leukemia. What was intriguing for us was that simply restoring Pax5 was enough to normalize these cancer cells, despite the other genetic changes.”

In leukemia, immature white blood cells replicate abnormally and build up in the bone marrow, interfering with production of normal blood cells.

Ms Liu said Pax5 was a gene frequently ‘lost’ in childhood B-ALL. “Pax5 is essential for normal development of a type of white blood cells called B cells,” she said. “When Pax5 function is compromised, developing B cells can get trapped in an immature state and become cancerous. We have shown that restoring Pax5 function, even in cells that have already become cancerous, removes this ‘block’, and enables the cells to develop into normal white blood cells.”

Dr Dickins said the research shed light on the function of Pax5, which was one of about 100 genes known to ‘suppress’ human tumors. “When these tumor suppressor genes are inactivated by changes to the DNA, cancers start to develop,” Dr Dickins said.

“This work shows how inactivating the tumor suppressor gene Pax5 contributes to B-ALL development and how leukemia cells become ‘addicted’ to low Pax5 levels to continue proliferating. Even though the B-ALL cells have multiple genetic mutations, simply reactivating Pax5 causes tumor cells to resume normal development and lose their cancerous properties.”

Dr Dickins said forcing B-ALL cells to resume their normal development could provide a new strategy for treating leukemia. “While B-ALL has a relatively good prognosis compared with other cancers, current treatments can last years and have major side-effects. By understanding how specific genetic changes drive B-ALL, it may be possible to develop more specific treatments that act faster with fewer side-effects.”

However Dr Dickins said that genes that are lost in tumor cells are not traditionally drug targets. “It is very difficult to develop drugs that restore the function of genes that are lost during cancer development,” Dr Dickins said. “However by understanding the mechanisms by which Pax5 loss causes leukemia, we can begin to look at ways of developing drugs that could have the same effect as restoring Pax5 function.”

The genetic switch technology used to study Pax5 could also be used to understand ‘tumour suppressor’ genes in other cancers, he said.

John Oliver interviews Stephen Hawking .


John Oliver talks to Stephen Hawking in the first installment of Last Week Tonight’s new “People Who Think Good” series. They cover such topics as parallel universes, artificial intelligence, and Charlize Theron.

watch the video: https://www.youtube.com/watch?feature=player_embedded&v=T8y5EXFMD4s

Oil Pulling – The Habit That Can Improve Your Oral Health


Oil pulling is an old healing treatment in which natural substances are used in the process of cleaning and detoxifying teeth and gums. It has whitening effect, too, and there is evidence that it improves the condition of gums and eliminates dangerous bacteria.

The oil pulling process includes swishing oil in the oral cavity for a short time each day, and this treatment is beneficial in improving oral health in general. Similar to the oil cleansing treatment for the skin, the principle of “like dissolves like” is applied here, as well, since oil is able to go through the plaque and remove toxins without any side-effects.

This treatment was first used in India thousands of years ago, and it was introduced to the US in the early 1990s, by dr. F. Karach, who has successfully been using the oil pulling process to treat his patients.

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There are hundreds of people sharing their experience online, including its benefits in treating skin problems, arthritis, asthma, headache, hormone imbalances, infections, liver problems and more.

Even though is widely used to treat all those health conditions, oil pulling is most often used in treating oral problems. On the recent Heal Thy Mouth Summit, a number of experts explained how bacteria can enter the blood through the mouth, and the possible infections can impact different parts of the body, which show perfectly why oral health is quite important.

oil-pulling-the-habit-that-can-improve-your-oral-health1

At the end, oil pulling has no side-effects as long as you use a high quality oil – good enough to be used in cooking. Oil pulling is not expensive at all, and it can provide great benefits regarding oral health, so there is no reason why you should not try it.

How to do Oil Pulling:

This treatment is amazingly simple. Swish a couple teaspoons of oil (coconut, sesame or olive oil) in the mouth and keep it for 20 minutes. Spit the oil out and rinse well. Oil pulling is best done in the morning, before having your meals or drinking anything, even though Dr. Bruce Fife suggests it can be done before every meal in cases of more severe infections or dental problems.

Step 1

Put 1 or 2 teaspoons of oil (preferably use coconut oil) in your mouth.. Most people prefer using 2 teaspoons of organic coconut oil. Use solid coconut oil and let it melt before swishing. You can also add a few drops of Brushing Blend (antibacterial).

 

 

Stress link to heart attack uncovered .


Chronic stress causes the overproduction of disease-fighting white blood cells, worsening inflammation in plaque in the arteries, shows a new study.

The finding may help explain how stress increases the risk of heart attacks, report scientists in the journal Nature Medicine.

Surplus cells clump together on the inner walls of arteries, restricting blood flow and encouraging the formation of clots that block circulation or break off and travel to another part of the body, say the study’s authors.

White blood cells “are important to fight infection and healing, but if you have too many of them, or they are in the wrong place, they can be harmful,” says study co-author Matthias Nahrendorf of the Harvard Medical School in Boston.

Doctors have long known that chronic stress leads to cardiovascular disease, but have not understood the mechanism.

To find the link, Nahrendorf and a team studied 29 medical residents working in an intensive care unit.

Their work environment is considered a model for chronic stress exposure given the fast pace and heavy responsibility they carry for life-and-death decisions.

Comparing blood samples taken during work hours and off duty, as well as the results of stress perception questionnaires, the researchers found a link between stress and the immune system.

Particularly, they noticed stress activate bone marrow stem cells, which in turn triggered overproduction of white blood cells, also called leukocytes.

Heart attack

White blood cells, crucial in wound healing and fighting off infection, can turn against their host, with devastating consequences for people with diseases like atherosclerosis — a thickening of artery walls caused by a plaque buildup.

The study then moved on to mice, which were exposed to the rodent equivalent of stress through techniques like crowding and cage tilting.

They found that excess white blood cells produced as a result of stress accumulated on the inside of arteries and boosted plaque growth in atherosclerosis-prone mice.

“Here, they (the cells) release enzymes that soften the connective tissue and lead to disruption of the plaque,” says Nahrendorf.

“This is the typical cause of myocardial infarction (heart attack) and stroke.”

He added leukocytes were only a part of the picture — factors like high cholesterol and blood pressure, smoking and genetic traits also contribute to heart attack and stroke risk.

“Stress might push these over the brink,” he says.

HowStuffWorks “Top 5 Crazy Government Experiments”


What comes to mind when you hear the words “government experiment”? If Google Image Search can truly gauge this sort of thing, then your head’s likely swimming with comic-book super soldiers, conspiracy theories, mutated animals and — oddly enough — country music singer Kenny Roger’s face.

Outside the world of comics and horror flicks, funding is pretty tight, especially for mad scientists. You’d be surprised how hard it is to snag a government grant when your proposal includes snippets like “a deep penetrating dive into the plasma pool” and “bow down before me.” As such, most government-funded research tends to stay away from atomic supermen.

Countless constructive, life-changing breakthroughs trace back to government-funded labs, from various vaccines to microwave ovens. The comfy insoles in your shoes, for instance, are just one everyday wonder brought to you by NASA.

Still, the occasional oddball premise slips past the people who control government grant applications. Regardless of the possible benefits to humanity, these are the government experiments that garner the most attention. After all, the prospect of genetically modified flying piranhas is troubling enough, but tack on “tax-funded” and you have a real public outcry on your hands.

In this article, we’ll leave behind the drive-in theaters and the horror aisles of the video store and breeze through five of the craziest real-life government experiments we could find.

 

 

http://science.howstuffworks.com/innovation/scientific-experiments/5-government-experiments.htm?mkcpgn=fb6&utm_source=facebook.com&utm_medium=social&utm_campaign=hswaccount

From the desk of Zedie.

To Solve The Water Problem, We Need To Solve Energy.


Within policy circles, people often bandy about the term “water-energy nexus.” Like most wonk-speak, it’s a rather complex way to express a simple relationship. Energy production requires a tremendous amount of water, almost on par with irrigated agriculture. And water production needs a lot of energy, for pumping, treating, and transportation. They’re interdependent. And therein lies the problem. We asked the U.S. Department of Energy’s Michael Knotek, the deputy under secretary for science and energy and a scientist himself, how to plan for a future in which we’ll demand a lot of both.

Why worry about the water-energy nexus anyway?

If you look around the world, the water-energy nexus is the first thing foreign governments talk about, particularly in developing countries. Over the next 40 years, we’re going to have a growing population and an evolving climate system. So we’ll be facing, almost in real time, a continually evolving set of challenges.

That could create big issues geopolitically. If you want to know where the big conflicts in the world are going to occur, you go to places that are right at the edge today. Take, for example, the parts of India and China that are currently dependent on very few sources of water. They could be impacted heavily by climate change. As the population grows and their economic productivity goes up, they’re going to be much closer to being at the crisis point than we are. Much closer.

What about here in the U.S.?

The western United States has similar issues. How are we going to manage water needs when the population’s growing and the climate models say the region will face serious problems? We have to prepare the whole country to deal with that. It may turn out that we have to move a lot of water around this country sometime in the next 30 to 50 years.

“We may have to move a lot of water around this country in the next 30 to 50 years.”

Where do we start?

The first thing we need to do is to look at the big challenges. Those go all the way from the materials underlying new technologies to systems analysis. But we also need enough data and data-management systems to understand the water-energy interface across this country. Once you understand it, the question is, What are you going to do about it?

What is the DOE doing about it?

We have a tech team around water-energy, which cuts across all of our programs. It also intersects with our national laboratory system. Desalination is big on the energy-for-water side of things. We’re also looking at new power systems for the thermo-electric cycle—for example, supercritical carbon dioxide as opposed to steam as a driver for the turbines on power plants.

Most renewables, except for hydropower, don’t need much water at all, if any.  And there’s a lot of recovered, or produced, water that turns out is very usable. In the case of fracking, where this water can be an issue, people have to learn how to use it again or treat it in another way.

Where does climate change fit in?

If you have a more climate-impacted world in the future, you’re going to have more droughts and floods. So everything is going to have to be hardened against extreme weather. That’s just going to be a feature of all our systems. Look at what happened with Hurricane Sandy. Whether it was or was not a climate change event is arguable, but what it did do was demonstrate the vulnerability of coastal populations and infrastructure. It just went in there and caused a mess.

What more can we do?

I’ve been working on the problem of new energy systems for 40-plus years. The mindset has always been that if you can understand the problems, you can solve them. But you’d better understand them first. And you’d better get a sense of urgency. We have to start preparing for the future. We can no longer just whistle past the graveyard.

From Autism to Anorexia, It’s All About the Gut .


Whether you suffer with a chronic illness, psychiatric disorder or psychological condition, the first thing to check is your belly.  All diseases begin in the gut,says Dr. Natasha Campbell-McBride, M.D., a leading expert on the subject of autism as well as other learning disabilities and digestive disorders.  In her work, she heals both mind and body by focusing on the health of the belly.

At her Cambridge Nutrition Clinic established in England in 1998, Dr. Campbell-McBride traces the connection between neurology and nutrition as well as digestion and the functioning of the rest of the body. “The digestive system holds the root of our health,” she says pointing out the extensive role that gut flora plays in disease prevention, including protecting us from invading pathogens, detoxification, facilitating the digestion of food as well as the absorption of vitamins and minerals like calcium and zinc, and actually producing B vitamins. In addition, between 84-88% of the immune system is housed in the gut lining, she says, which would equal the size of a tennis court if opened up and laid flat .

There cannot be cancer in the digestive tract if the gut flora is healthy,” asserts Dr. Campbell-McBride, a medical doctor with postgraduate degrees in both neurology and human nutrition. But in today’s society, many people are walking around with impaired gut flora due to steroids, prescription medications, alcohol, stress, a poor diet of processed foods and sugar (which actually feed abnormal gut flora), disease, age, bottle feeding of infants, toxic chemicals, pollution and radiation.

How Antibiotics Can Lead to Mercury Poisoning

A major cause of impaired gut flora are antibiotics and she worries about teenagers being treated for up to two years with acne drugs, leaving them with serious damage.

From Autism to Anorexia, It's All About the Gut

Dr. Campbell-McBride points to a study showing that rats treated with antibiotics succumb to mercury poisoning while those with untreated gut flora do not. She believes the same is true of humans and that, while the government warns against eating fish because of mercury and PCB contamination, a healthy gut should be able to tolerate the exposure and get the health benefits of eating fish.

Gut Health and the Autism Epidemic

According to Dr. Campbell-McBride, as a population we are degrading healthy gut flora more and more every generation. Mothers who have been on the Pill or antibiotics or a poor diet for long periods develop abnormal gut flora and pass it on to their children. This, she believes, has led to an epidemic of eczema and autism, noting that 20 years ago the autism rate was 1 in 10,000 children and today is 1 in 88.

When children are born with their mothers’ unhealthy gut, they have immune compromised systems, develop ear and chest infections and are treated with antibiotics.  All this creates more damage to their systems. As the gut wall suffers more damage, it becomes “leaky” and allows undigested food to enter the blood stream resulting in more prevalent food allergies, such as to peanuts.

The Surprising Power of Silence .


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It’s easy to think of moments in our favorite music that are silent, but expressively powerful: that second before a classical pianist puts her hands on the keyboard; the stop taken by a rock band just before a song’s climax. Competing lists vie to chronicle the best musical pauses of all time—Jennifer Egan even wrote a book inspired by their power.

People seem to generally agree that the right pause at the right time can knock our socks off.

 

Musical pauses can also help us understand what listeners are doing when they listen to music. If there’s a two-second pause in one song that we hardly notice and a two-second pause in another that blows our mind, then we know that listening isn’t just a matter of passively receiving the most recent acoustic event: in each case, the most recent event was two seconds of nothing at all.

Instead, responses to pauses help show us that musical listening is actually quite active, with listeners listening ahead and making predictions about what might come next. If a pause happens when listeners are expecting it—at the end of a phrase, for example—they might hardly notice, but if the same pause occurs at a surprising moment—midphrase, just before the climax, on a downbeat—listeners might find chills creeping down their backs.

In 2007, I ran a study of participants who hadn’t had any formal musical training—exactly the type of people who normally swear they don’t know anything about music. But their responses to musical pauses showed that they know a lot more than they think. In the experiment, participants pressed buttons when pauses began and ended; moved a slider to increase perceptions of dynamic fluctuations in tension and relaxation as the music (and pauses) progressed; and estimated they length of the pauses they’d heard.

Despite the fact these listeners were generally unfamiliar with the notion of tonal closure, their responses revealed that it played a large role in their perceptions. Broadly speaking, tonal closure involves a return to the tonic—the home note of the current key. When a pause followed tonal closure, people took longer to register that a silence had started—it was so expected as to be almost invisible. But when a pause preceded tonal closure, people were startled, and able to report right away that a silence had happened.

When a pause occurred before tonal closure, people also reported experiencing the silence as tense and expressively fraught. They even thought it lasted longer than it really had.

Because they’re empty of sound, these silent periods are excellent windows into the active and predictive engagement listeners sustain within pieces of music. This engagement continues beyond the pauses, characterizing the way even people without any formal training process music. But it’s the silent moments that show us how powerful tonal adventures can be—powerful enough to make even silence musical.