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Aspirin ‘Helps Protect Against Bowel Cancer’

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A daily aspirin tablet may help prevent bowel cancer, a study suggests.

Oxford University found it cut cases by a quarter and deaths by more than a third in a review of 14,000 patients.

Aspirins are already widely used to help protect people against strokes and heart problems, although many healthy middle-aged people do not take them because of the risk of side-effects.

But researchers said their findings – published by the Lancet – “tipped the balance” in favour of taking them.

They followed up four study groups over a period of 20 years to identify the impact of regular small doses of of the drug – the tablets given for medical reasons are often a quarter of a strength of those used to treat headaches.

They found it reduced the risk of the incidence of bowel cancer by 24% and of dying from the disease by 35%.

And even though regular aspirin use can have side-effects, the researchers said it was still worthwhile as on such low doses these tended to be relatively minor, such as bruising or nose bleeds.

One in 20 people in the UK develops bowel cancer over their lifetime, making it the third most common cancer. About 16,000 people die each year as a result of it.

The findings build on previous research on the issue, and come after the government announced earlier this month it was looking to start a new screening programme for bowel cancer for 55-year-olds.

Lead researcher Professor Peter Rothwell said the screening would provide the perfect opportunity for doctors to discuss with their patients about whether to take aspirin.
He said:-“To date, for healthy middle-aged people it has been a fine balance as to whether to take aspirins, but this tips it in my view.

“There is a small benefit for vascular disease and now we know a big benefit for this cancer. In the future, I am sure it will be shown that aspirin helps prevent other cancers too.”

‘Talk to GP

He added those with a high risk of bowel cancer, including the obese and those with a family history of the disease, should give aspirin treatment a particular consideration.

Mark Flannagan, chief executive of Beating Bowel Cancer, said they were “very positive” findings and giving aspirin alongside the new screening programme should be looked at.

But he added: “Anyone considering starting a course of medication should first consult their GP.”

You may click to see :Bowel cancer risk gene pinpointed

Source : BBC News

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Second Time Dengu Attack Spells Danger

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Scientists now know why a second dengue infection is much more severe than the first.
The long-kept secrets of the dengue virus — which affects between 50 and 100 million people every year — are tumbling out.

Scientists have long wondered why a re-infection (in the same or subsequent year) causes more complications, even becoming fatal, than when it strikes the first time. The puzzle has been finally solved — by two independent research teams. The knowledge gained by the scientists is expected to help design drugs and vaccines against dengue fever, which currently has no treatment.

Normally, viruses — which have very little genetic material of their own — co-opt the host’s genetic machinery to survive and replicate. More often than not, if the host has an efficient immune system, the invaders are destroyed. In most cases, the antibodies produced by the body stay for long, if not permanently, and fight off any subsequent attack by the same virus. But in the case of dengue, the second infection proves to be much more severe than the first.

Back in the 1970s, US virologist Scott Halstead hypothesised that the dengue virus may be receiving help from the very antibodies that are supposed to fight the infection. Halstead termed the phenomenon antibody-dependent enhancement (ADE) of infection. He got an inkling of this during his extensive clinical studies in Thailand in the 1960s.

For a good part of the ensuing four decades, Halstead’s assumption remained mere theory. But in February this year, Sujan Shresta, a Nepal-born virologist at the La Jolla Institute of Allergy and Immunology in California, came up with conclusive proof for Halstead’s hypothesis. “It’s a situation where antibodies can be bad for you — it’s counter to everything we know about the normal function of antibodies,” she says.

Dengue infection is transmitted by the Aedes aegypti mosquito. There are four known strains of the virus circulating in the world. Infection can cause diseases ranging from dengue fever, a flu-like illness, to the severest form — dengue haemorrhagic fever or dengue shock syndrome. The latter can cause the blood vessels to leak, leading to life-threatening shock. It is estimated that 2.5 billion people — that is, two-fifth of the world’s population — live in regions where dengue fever is rampant. While it is more common in South East Asia and South America, the incidence is rising in India too. Since 1996, the country had witnessed a number of dengue outbreaks and a few hundred Indians die of dengue-related complications every year.

Shresta’s team at La Jolla developed the first ever mouse model to study the disease. The scientists conducted experiments to prove that certain antibodies produced by the body against the virus indeed exacerbate the condition. The four strains of the virus circulate simultaneously, says Shresta. Infection with one provides lifelong immunity against that particular strain. In subsequent infections, where a different strain of the virus is involved, the antibodies do not recognise enough of the virus to neutralise it. “This starts a cascade of unusual molecular events — the ADE process — which leads to the antibodies contributing to, rather than fighting, the infection,” she explains.

Taking the research forward, a team of UK and Thai scientists identified specific antibodies involved in the ADE process. The study, reported early this month in the journal Science, showed that the culprits are antibodies against a particular viral protein called precursor membrane protein (prM). According to the researchers, if the antibodies are present in the body, the infection spreads faster with the antibodies against prM helping the virus infect more host cells. In fact, there is a several hundred-fold increase in the number of infected cells in the presence of the antibodies, they say.

“This is a significant piece of work. It shows the exact region for the enhancement — which is the prM, and not the E region of the virus, as we have been thinking so long,” says Shamala Devi Sekaran, a virologist at the University of Malaysia who has been studying the dengue virus for years.

“The study pinpoints the nature of the antibodies that are likely to cause the severest form of the disease in humans,” says Shresta. It will greatly help those trying to develop vaccines against dengue, she adds.

“Our research gives us some key information about what is not likely to work when trying to combat the virus. We hope our findings will bring scientists one step closer to creating an effective vaccine,” says Gavin Screaton, head of medicine, Imperial College London, and lead author of the study.

The biggest challenge is that the dengue vaccine will need to provide immunity against all the four strains of the virus at the same time. “If protection is incomplete, the vaccine can potentially protect against some viruses but leave the individual primed for a more severe outcome if he or she is infected with the others,” Screaton told Knowhow.

In addition to these developments, there have been two recent breakthroughs in controlling the dengue mosquito. Oxford University scientists developed sterile male Aedes aegypti mosquitoes which have undergone successful semi-field trials in Asia. And scientists at the University of Queensland developed a mutant strain of a bacterium called Wolbachia, which halves the adult life span of female Aedes aegypti mosquitoes in laboratory conditions.

The Teleghraph ( Kolkata, India)

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Another ‘Bad’ Cholesterol Linked to Heart Disease Found

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Scientists say they have found proof that another “bad” type of cholesterol contributes to heart disease.

Home testing kits can check for high cholesterol, but not Lp(a) specifically
Unlike the well-known LDL cholesterol, lipoprotein(a) or Lp(a) cannot be controlled by cutting down on dietary fats or taking a statin drug.

But researchers say high levels do not carry the same risk as LDL.

And other drugs might work to minimise its effects, they told the New England Journal of Medicine.

LDL is considered the aggressive tiger of the cholesterol world, furring the arteries and greatly increasing heart risk. Scientist believe Lp(a), which is inherited, is more of a pussycat, although it does appear to upset blood clotting.

Inherent risk:-
The researchers used gene-chip technology to scan DNA that they knew from previous studies were potential “hotspots” for heart disease risk. This analysis revealed the two genetic culprits.

Professor Martin Farrall, lead author of the study carried out at Oxford University, said one in six people carries one or more of the genes for Lp(a).

He said: “The increase in risk to people from high Lp(a) levels is significantly less severe than the risk from high LDL cholesterol levels.

“So Lp(a) doesn’t trump LDL, which has a larger impact and which we can already control pretty effectively.

“The hope now is that by targeting both we could get even better risk reduction.”

Some existing drugs, such as Niacin, and others coming on to the market, such as CETP-inhibitors, lower Lp(a) as well as LDL cholesterol.

Professor Peter Weissberg of the British Heart Foundation, which funded the study, said the findings were useful but urged people not to be alarmed by them.

“They highlight the importance of trying to lower Lp(a), which will spark new efforts to design a medicine to achieve this effectively.

“And they reveal clues that open a new avenue for research to decipher how heart disease develops.

“But LDL is still the type of cholesterol to be more concerned about.”

Fats from food are turned into cholesterol by the liver. There are different types but some, such as LDL, are known as “bad” cholesterol. They can lead to a build-up in the body’s cells.

Prof Weissberg said everyone could reduce their risk of heart disease by eating a healthy balanced diet, being physically active and avoiding smoking.

Source: BBC News:Dec. 24.’09

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Fountain of Youth from Chemicals of Easter Island Soil

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A miraculous ‘elixir of youth’ which could extend the human life span by more than a decade is being developed by scientists.
The anti-ageing pill was created from a chemical found in the soil of Easter Island –  one of the most remote and mysterious places on the planet.

In tests on animals, the chemical increased life expectancy by a staggering 38 per cent.

While the breakthrough sounds like something out of science fiction, scientists say the discovery is a major leap towards longer lives for everyone.

The drug, rapamycin, is already used to suppress the immune systems of organ transplant patients.

It is also employed in heart operations and is being tested for its anti-cancer properties.

The scientists believe that the drug could be developed within a decade.

Dr Arlan Richardson, who led the research at the University of Texas, said: ‘I never thought we would find an anti-ageing pill for people in my lifetime. However, rapamycin shows a great deal of promise to do just that.’

An anti-ageing pill is a Holy Grail for medical research and its development would have major repercussions for society.

In a world where people routinely live to 90 and 100, retirement ages would need to creep forward into the 70s while extended life spans would put enormous pressures on healthcare, housing and social services  –  as well as marriages.

The implications of a such a pill also depends on the quality of those extra years.

If an ageing drug delays every aspect of getting old, then users could enjoy 100 years of good health.

But if it simply postpones death, they could find their last few decades blighted by failing eyesight, hearing loss, frailty and dementia.
Rapamycin was discovered in the 1970s during a worldwide search for new antibiotics.

The chemical is produced by a microbe that lives in the Easter Island soil.
In its current form, the drug is too dangerous to hand out as an anti-ageing pill.

The compound suppresses the immune system and makes patients vulnerable to any viruses and bacteria.

The existing version of the drug also increases the risk of cancer and would need to be modified before using in human trials.

However, researchers believe the new discovery will lead them to similar  –  but less harmful  –  anti-therapies.

In the study, reported today in the journal Nature, scientists tested rapamycin on nearly 2,000 laboratory mice aged around 600 days  –  roughly the equivalent to a 60-year-old person.

Around a quarter of the mice were given a normal diet, the others the Easter Island chemical.
Land of mythical statues: Easter Island soil provided the anti-ageing chemical
The drug increased the maximum life span of the mice from 1,094 days to 1,245 days for females, and from 1,078 to 1,179 days for males.
From the point the mice began the treatment, the drug extended the females’ life expectancy by 38 per cent, and males by 28 per cent. Overall it expanded their life span by 9 to 14 per cent.

What amazed the scientists is that the drug worked even though the mice started to be given it only in middle and old age.

Until now, scientists have developed just two ways of extending the life span of mammals.

One is to tinker with their genes, the other to restrict their diet.

Repeated studies have shown that cutting calories can make animals and people live longer.

Experts believe that rapamycin  –  which acts on a protein in cells called TOR  –  might fool the body into thinking that calories are being restricted. British scientists described the findings as exciting  –  but stressed that rapamycin weakens the immune system, exposing patients to potentially dangerous diseases.

In its current form, an extended life span would come at the cost of having to live in a germ-free tent.

Researchers want to find another more subtle drug target that extends life, but which does not damage the immune system.

Dr Lynne Cox, researcher in ageing at Oxford University, said: ‘In no way should anyone consider using this particular drug to try to extend their own life span as rapamycin suppresses immunity. While the lab mice were protected from infection, that’s simply impossible in the human population.

‘What the study does is to highlight an important molecular pathway that new, more specific drugs might be designed to work on.

‘Whether it’s a sensible thing to try to increase life span this way is another matter: Perhaps increasing health span rather than overall life span might be a better goal.’

Source:Mail Online July 9. 2009

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The Origins of Swine Flu Revealed

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 A new research has revealed the origins of swine flu after scientists discovered that the transmission of the H1N1 influenza A virus to humans occurred several months before recognition of the existing outbreak.

India has confirmed a total of 23 cases of swine flu in the country, with the World Health Organisation declaring the outbreak as a pandemic.

In the new research, an international team, led by Oxford University, used evolutionary analysis to estimate the timescale of the origins as well as the early development
of the swine flu pandemic.

According to the scientists, the virus was actually derived from several viruses circulating in swine, and that the initial transmission to humans occurred several months before recognition of the outbreak.

Lead scientist Dr Oliver Pybus said, “Using computational methods, developed over the last ten years at Oxford, we were able to reconstruct the origins and timescale of this new pandemic.”

“Our results show this strain has been circulating among pigs, possibly among multiple continents, for many years prior to its transmission to humans.”

The research highlights the need for systematic surveillance of influenza in swine, and provides evidence that new genetic elements in swine can result in the emergence of viruses with pandemic potential in humans.

The scientists concluded that “despite widespread influenza surveillance in humans, the lack of systematic swine surveillance allowed for undetected persistence and evolution of this potentially pandemic strain for many years.”

The team included scientists from Oxford University, the University of Edinburgh, the University of Hong Kong and the University of Arizona. Their findings are published in the latest edition of the ‘Nature’ journal.

Source: The Times Of India

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