Moral of story?
Stop smoking, lose weight, and eat your greens.
For the full feature story n BBC News, go to: http://www.bbc.co.uk/news/health-16031149
Wednesday, 7 December 2011
Over 40% of cancers due to lifestyle
Finally, someone publishes a comprehensive study on the causes of cancer. The work of Prof Max Parkin from Wolfson Institute of Preventive Medicine, published in the British Journal of Cancer, was featured in BBC News Heath section.
Moral of story?
Stop smoking, lose weight, and eat your greens.
For the full feature story n BBC News, go to: http://www.bbc.co.uk/news/health-16031149
Moral of story?
Stop smoking, lose weight, and eat your greens.
For the full feature story n BBC News, go to: http://www.bbc.co.uk/news/health-16031149
Tuesday, 1 November 2011
You're one in 7 billion
From Wired Science by Brandom Keim: Making Sense of 7 Billion People
On the last day of October 2011, the global population of an upstart branch of the primate order will reach 7 billion.
What does it mean?
In itself, not much: Seven billion is just a one-digit flicker from 6,999,999,999. But the number carries a deep existential weight, symbolizing themes central to humanity’s relationship with the rest of life on Earth.
For context, let’s consider a few other numbers. The first: 10,000. That’s approximately how many Homo sapiens existed 200,000 years ago, the date at which scientists mark the divergence of our species from the rest of Homo genus, of which we are the sole survivors.
From those humble origins, humans — thanks to our smarts, long-distance running skills, verbal ability and skill with plants — proliferated at an almost inconceivable rate.
Some may note that, in a big-picture biological sense, humanity has rivals: In total biomass, ants weigh as much as we do, oceanic krill weigh more than both of us combined, and bacteria dwarf us all. Those are interesting factoids, but they belie a larger point.
Ants and krill and bacteria occupy an entirely different ecological level. A more appropriate comparison can be made between humans and other apex predators, which is precisely the ecological role humans evolved to play, and which — beneath our civilized veneer — we still are.
According to a back-of-the-envelope calculation, there are about 1.7 million other top-level, land-dwelling, mammalian predators on Earth. Put another way: For every non-human mammal sharing our niche, there are more than 4,000 of us.
In short, humans are Earth’s great omnivore, and our omnivorous nature can only be understood at global scales. Scientists estimate that 83 percent of the terrestrial biosphere is under direct human influence. Crops cover some 12 percent of Earth’s land surface, and account for more than one-third of terrestrial biomass. One-third of all available fresh water is diverted to human use.
Altogether, roughly 20 percent of Earth’s net terrestrial primary production, the sheer volume of life produced on land on this planet every year, is harvested for human purposes — and, to return to the comparative factoids, it’s all for a species that accounts for .00018 percent of Earth’s non-marine biomass.
We are the .00018 percent, and we use 20 percent. The purpose of that number isn’t to induce guilt, or blame humanity. The point of that number is perspective. At this snapshot in life’s history, at — per the insights of James C. Rettie, who imagined life on Earth as a yearlong movie — a few minutes after 11:45 p.m. on December 31, we are big. Very big.
However, it must be noted that, as we’ve become big, much of life had to get out of the way. When modern Homo sapiens started scrambling out of East Africa, the average extinction rate of other mammals was, in scientific terms, one per million species years. It’s 100 times that now, a number that threatens to make non-human life on Earth collapse.
In regard to that number, environmentalists usually say that humanity’s fate depends on the life around us. That’s debatable. Humans are adaptable and perfectly capable of living in squalor, without clean air or clean water or birds in the trees. If not, there wouldn’t be 7 billion of us. Conservation is a moral question, and probably not a utilitarian imperative.
But the fact remains that, for all of humanity to experience a material standard of living now enjoyed by a tiny fraction, we’d need four more Earths. It’s just not possible. And that, in the end, is the significance of 7 billion. It’s a challenge.
In just a few minutes of evolutionary time, humanity has become a force to be measured in terms of the entirety of life itself. How do we, the God species, want to live? For the answer, check back at 8 billion.
From sfgate.com
Lagos, Nigeria -- One South African mother, just 19, named her newborn "Enough" and shrugged off a nurse who questioned whether she was old enough to know how many children she wanted.
In Nigeria, newborn twins have to share a bassinet in a crowded public hospital that doesn't have enough electricity.
"Where there is life, there is hope," their mother said. But as the world's population surpasses 7 billion, fears were stirred anew about how the planet will cope with the needs of so many humans.
The United Nations marked the milestone Monday, even though it is impossible to pinpoint the arrival of the globe's 7 billionth occupant because millions of people are born and die each day.
At Lagos Island Maternity Hospital, the strain of caring for a burgeoning population was evident. The droning roar of a generator could be heard throughout one hot ward, where it powered ceiling fans and incubators. While Nigeria is oil-rich, it does not produce nearly enough power for its more than 160 million people.
Nigeria's megacity of Lagos is expected someday to surpass Cairo as the continent's most populous.
U.N. Secretary-General Ban Ki-moon said the day was "not about one newborn or even one generation" but "about our entire human family."
At a news conference in New York, he noted "a world of contradictions" - famine in the Horn of Africa, fighting in Syria and elsewhere and widespread protests against economic inequality.
"Seven billion population is a challenge," he said, and "at the same time, an opportunity, depending upon how the international community prepares for that challenge."
Demographers say it took until 1804 for the world to reach its first billion people and a century more until it hit 2 billion in 1927. Soon the numbers began to cascade: 3 billion in 1959, 4 billion in 1974, 5 billion in 1987, 6 billion in 1998.
The United Nations estimates the world population will reach 8 billion by 2025 and 10 billion by 2083. But the numbers could vary widely, depending on life expectancy, access to birth control, infant mortality rates and other factors.
India, which struggles with a deeply held preference for sons and a skewed sex ratio because of millions of aborted female fetuses, is using the day to highlight that issue.
"It would be a fitting moment if the 7 billionth baby is a girl born in rural India," said Dr. Madhu Gupta, a gynecologist. "It would help in bringing the global focus back on girls, who are subject to inequality and bias."
According to U.S. government estimates, India has 893 girls for every 1,000 boys at birth, compared with 955 girls per 1,000 boys in the United States.
Meanwhile, China, which at 1.34 billion people is the world's most populous nation, said it would stand by its one-child policy, a set of restrictions launched three decades ago limiting most urban families to one child and most rural families to two.
"Overpopulation remains one of the major challenges to social and economic development," Li Bin, director of the State Population and Family Planning Commission, told the official Xinhua News Agency. India, with 1.2 billion people, is expected to overtake China around 2030, when the Indian population reaches an estimated 1.6 billion.
On the last day of October 2011, the global population of an upstart branch of the primate order will reach 7 billion.
What does it mean?
In itself, not much: Seven billion is just a one-digit flicker from 6,999,999,999. But the number carries a deep existential weight, symbolizing themes central to humanity’s relationship with the rest of life on Earth.
For context, let’s consider a few other numbers. The first: 10,000. That’s approximately how many Homo sapiens existed 200,000 years ago, the date at which scientists mark the divergence of our species from the rest of Homo genus, of which we are the sole survivors.
From those humble origins, humans — thanks to our smarts, long-distance running skills, verbal ability and skill with plants — proliferated at an almost inconceivable rate.
Some may note that, in a big-picture biological sense, humanity has rivals: In total biomass, ants weigh as much as we do, oceanic krill weigh more than both of us combined, and bacteria dwarf us all. Those are interesting factoids, but they belie a larger point.
Ants and krill and bacteria occupy an entirely different ecological level. A more appropriate comparison can be made between humans and other apex predators, which is precisely the ecological role humans evolved to play, and which — beneath our civilized veneer — we still are.
According to a back-of-the-envelope calculation, there are about 1.7 million other top-level, land-dwelling, mammalian predators on Earth. Put another way: For every non-human mammal sharing our niche, there are more than 4,000 of us.
In short, humans are Earth’s great omnivore, and our omnivorous nature can only be understood at global scales. Scientists estimate that 83 percent of the terrestrial biosphere is under direct human influence. Crops cover some 12 percent of Earth’s land surface, and account for more than one-third of terrestrial biomass. One-third of all available fresh water is diverted to human use.
Altogether, roughly 20 percent of Earth’s net terrestrial primary production, the sheer volume of life produced on land on this planet every year, is harvested for human purposes — and, to return to the comparative factoids, it’s all for a species that accounts for .00018 percent of Earth’s non-marine biomass.
We are the .00018 percent, and we use 20 percent. The purpose of that number isn’t to induce guilt, or blame humanity. The point of that number is perspective. At this snapshot in life’s history, at — per the insights of James C. Rettie, who imagined life on Earth as a yearlong movie — a few minutes after 11:45 p.m. on December 31, we are big. Very big.
However, it must be noted that, as we’ve become big, much of life had to get out of the way. When modern Homo sapiens started scrambling out of East Africa, the average extinction rate of other mammals was, in scientific terms, one per million species years. It’s 100 times that now, a number that threatens to make non-human life on Earth collapse.
In regard to that number, environmentalists usually say that humanity’s fate depends on the life around us. That’s debatable. Humans are adaptable and perfectly capable of living in squalor, without clean air or clean water or birds in the trees. If not, there wouldn’t be 7 billion of us. Conservation is a moral question, and probably not a utilitarian imperative.
But the fact remains that, for all of humanity to experience a material standard of living now enjoyed by a tiny fraction, we’d need four more Earths. It’s just not possible. And that, in the end, is the significance of 7 billion. It’s a challenge.
In just a few minutes of evolutionary time, humanity has become a force to be measured in terms of the entirety of life itself. How do we, the God species, want to live? For the answer, check back at 8 billion.
From sfgate.com
Lagos, Nigeria -- One South African mother, just 19, named her newborn "Enough" and shrugged off a nurse who questioned whether she was old enough to know how many children she wanted.
In Nigeria, newborn twins have to share a bassinet in a crowded public hospital that doesn't have enough electricity.
"Where there is life, there is hope," their mother said. But as the world's population surpasses 7 billion, fears were stirred anew about how the planet will cope with the needs of so many humans.
The United Nations marked the milestone Monday, even though it is impossible to pinpoint the arrival of the globe's 7 billionth occupant because millions of people are born and die each day.
At Lagos Island Maternity Hospital, the strain of caring for a burgeoning population was evident. The droning roar of a generator could be heard throughout one hot ward, where it powered ceiling fans and incubators. While Nigeria is oil-rich, it does not produce nearly enough power for its more than 160 million people.
Nigeria's megacity of Lagos is expected someday to surpass Cairo as the continent's most populous.
U.N. Secretary-General Ban Ki-moon said the day was "not about one newborn or even one generation" but "about our entire human family."
At a news conference in New York, he noted "a world of contradictions" - famine in the Horn of Africa, fighting in Syria and elsewhere and widespread protests against economic inequality.
"Seven billion population is a challenge," he said, and "at the same time, an opportunity, depending upon how the international community prepares for that challenge."
Demographers say it took until 1804 for the world to reach its first billion people and a century more until it hit 2 billion in 1927. Soon the numbers began to cascade: 3 billion in 1959, 4 billion in 1974, 5 billion in 1987, 6 billion in 1998.
The United Nations estimates the world population will reach 8 billion by 2025 and 10 billion by 2083. But the numbers could vary widely, depending on life expectancy, access to birth control, infant mortality rates and other factors.
India, which struggles with a deeply held preference for sons and a skewed sex ratio because of millions of aborted female fetuses, is using the day to highlight that issue.
"It would be a fitting moment if the 7 billionth baby is a girl born in rural India," said Dr. Madhu Gupta, a gynecologist. "It would help in bringing the global focus back on girls, who are subject to inequality and bias."
According to U.S. government estimates, India has 893 girls for every 1,000 boys at birth, compared with 955 girls per 1,000 boys in the United States.
Meanwhile, China, which at 1.34 billion people is the world's most populous nation, said it would stand by its one-child policy, a set of restrictions launched three decades ago limiting most urban families to one child and most rural families to two.
"Overpopulation remains one of the major challenges to social and economic development," Li Bin, director of the State Population and Family Planning Commission, told the official Xinhua News Agency. India, with 1.2 billion people, is expected to overtake China around 2030, when the Indian population reaches an estimated 1.6 billion.
Tuesday, 18 October 2011
The HWANG strikes back!
From The Telegraph:
Hwang Woo-suk, who was stripped of his stem cell research license in 2006 over ethical issues now claims to have successfully cloned eight coyotes using techniques he developed in the first cloning of a dog in 2005.
Hwang Woo-suk, who was stripped of his stem cell research license in 2006 over ethical issues now claims to have successfully cloned eight coyotes using techniques he developed in the first cloning of a dog in 2005.
"We injected a coyote's somatic cell into a dog's egg and produced a cloned embryo. The pups were born 60 days after we transplanted the embryo into the dog's uterus," he said.
Convicted of fraud and embezzling state funds in 2009, Hwang's disgrace set back South Korea's stem cell research by years after two journal papers hailed as landmark studies were found to have based on fabricated data.
Hwang, who has always denied any wrongdoing said he hoped to apply his procedure to bring back extinct animals in future.
"After six years of innovation, the success rate is now at 50 percent. We want to apply the cloning skills we acquired from working with dogs, to animals that are in danger of extinction," he said.
http://www.telegraph.co.uk/science/8831510/Disgraced-scientist-claims-coyote-cloning.html
http://www.telegraph.co.uk/science/8831510/Disgraced-scientist-claims-coyote-cloning.html
Wednesday, 21 September 2011
Fear not thy wrinkles
Article from New Scientist 21 September 2011 by Andy Coghlan
BEAUTY may be no more than skin-deep, but many of us think that leaves plenty of room for improvement. So a new dietary treatment that promises to shrink wrinkles from inside the skin is bound to be big news when it is launched next month.
The makers of the three-a-day capsules say they use blends of natural food extracts to activate genes that improve skin tone - and early results suggest they may be on the right track.
If the results stand up to scrutiny, the capsules will be the first anti-wrinkle treatment to show evidence of combating wrinkling from the deeper layers of skin. But they will not be the first to win scientific backing - some skin creams have been shown in peer-reviewed journals to help reduce wrinkles (British Journal of Dermatology, DOI: 10.1111/j.1365-2133.2009.09436.x).
Independent researchers contacted by New Scientist said that the preliminary results are intriguing and commended the team developing the capsules for conducting a double-blind trial - testing them against a placebo with neither researchers nor recipients knowing until afterwards who had received what. They say they will be sceptical, however, until a peer-reviewed journal has published the results in full, and acknowledge that attempts to erase the signs of ageing don't sit well with everyone.
The "gene food" treatment is the work of John Casey's team at the laboratories of Unilever in Sharnbrook, UK. The multinational food, cosmetics and household products company commissioned four separate research groups to test the capsules, and 480 women in the UK, France and Germany who have passed the menopause took part in the trials.
New Scientist has seen results that show that in 14 weeks, "crow's feet" wrinkles by the corner of the eye became on average 10 per cent shallower in recipients of the capsules, shrinking by 30 per cent in the best responders.
The wrinkles of women who received a placebo did not change significantly in depth.
In one of the two French studies, researchers also took 4-millimetre-deep biopsies from 110 women before and after treatment to study the production of collagen - a protein that is a key structural component of skin. Antibodies that stain tissue red where new collagen is produced revealed that after treatment a fifth of recipients had significantly more fresh collagen in the deepest skin layer - the dermis - than those who had received a placebo. More sensitive tests will be needed to ascertain any differences in the remaining biopsies, says Casey. Partial results were presented at the Society for Investigative Dermatology meeting in Atlanta, Georgia, last year; Casey says that the full data will now be sent to journals for peer review.
So how do these capsules work? As women age and oestrogen production drops off towards menopause, enzymes called proteases become more active, reducing the sponginess of skin by clearing away collagen faster than it can be replaced. An oestrogen receptor that aids the generation of collagen also becomes less active. The two effects combine to make skin less pliable and more wrinkly.
Casey's team used skin cultures and gene activity tests to ascertain the effect of certain natural food extracts on "master" genes, which orchestrate the behaviour of lots of other genes - in this case, those involved in collagen synthesis. The blend that activated these genes most strongly included vitamins C and E plus isoflavones from soya, lycopene from tomatoes and omega-3 polyunsaturated acids from fish oil.
Unilever plans to launch the product next month in 44 spas that it co-owns in the UK, Spain and Canada. It does not need approval to sell the capsules from these countries' regulatory authorities because the extracts they contain are already in use and the company does not claim that the capsules benefit health.
Although long-term tests have not been carried out, Gail Jenkins, another member of the team, recommends taking three capsules per day for at least three months; at this dose, she says, adverse side effects are unlikely. If a person stopped taking the capsules, the normal ageing process would probably restore deeper wrinkles.
When New Scientist sent the preliminary data to independent dermatologists, they gave a guarded welcome. "The data are somewhat sparse, but they do appear to have done a pretty comprehensive study," says Christopher Griffiths, professor of dermatology at the University of Manchester, UK, and co-author of a 2009 study confirming that an anti-ageing cream produced by Boots, a British pharmacy chain, had anti-wrinkle effects (British Journal of Dermatology, DOI: 10.1111/j.1365-2133.2009.09216.x). Griffiths said he would be "unconvinced" until he had seen all the data, but was intrigued by the apparent repair of deep rather than superficial wrinkles. "I know of no other study that has shown this before," he says. A likely explanation, says Casey, is that creams penetrate only the top layer of skin - the epidermis. The contents of the capsules, by contrast, reach the dermis, stimulating the production of collagen in deeper layers.
Richard Weller, a dermatologist at Edinburgh Royal Infirmary, UK, applauded Unilever for testing the product against a placebo and for saying it will publish the results in full. "What matters is the clinical data, and they show there are reduced wrinkles in the treated group," he says. "I'm not aware of any [other] oral treatments that do this."
David Sarwer of the University of Pennsylvania, Philadelphia, says that the results are encouraging but "we need a number of studies in this area, with similar results and published in the peer-reviewed literature, before we have a sufficient body of evidence to suggest that these supplements positively impact facial appearance".
Nichola Rumsay of the Centre for Appearance Research at the University of the West of England in Bristol says that anti-wrinkle capsules are more psychologically benign than facial surgery, but they still reinforce the message that wrinkles are bad. "We should be accepting wrinkles gracefully. Someone should develop a pill to stop people worrying about their appearance," she says. "That would make people a lot happier."
I like Nichola Rumsay's comment. What's wrong with wrinkles?! With wisdom, poise and class, you can look great at any age.
Tuesday, 13 September 2011
What's the image of a scientist in your head?
If you were to ask someone to draw a scientist, most likely you would get a picture of a man with frizzy hair, crazy expression, wearing a white lab coat, and holding a test-tube.
Something like this:
Or this:
Even well known TV science presenters like physicist Dr Brian Cox and naturalist Sir David Attenborough could not debunk the impression that people have of scientists.
Well, let's set things straight.
Myth #1: Scientists are men
Dr Rosalind Franklin, British Biophysicist and X-ray crystallographer, made critical contribution to the understanding of the structure of DNA.
Myth #2: Scientists are ugly
Something like this:
 | ||
| Albert Einstein |
 |
| Charles Darwin |
Even well known TV science presenters like physicist Dr Brian Cox and naturalist Sir David Attenborough could not debunk the impression that people have of scientists.
Well, let's set things straight.
Myth #1: Scientists are men
Dr Rosalind Franklin, British Biophysicist and X-ray crystallographer, made critical contribution to the understanding of the structure of DNA.
Myth #2: Scientists are ugly
Dr Kevin Eggan, associate professor of stem cell and regenerative medicine at Harvard, was featured in People Magazine as one of the sexiest men alive!
Myth #3: Scientists are geek freaks who only know science
Leonardo Da Vinci was an expert mathematician, engineer, inventor, anatomist, painter, sculptor, architect, botanist, musician and writer. Nuff said.
One point I can't debunk though, is that scientists are indeed, CRAZY.
 |
| Institute christmas party 2006 |
 |
| Institute christmas party 2007 |
 |
| Labmates and I at "bad taste" party 2011 |
Monday, 12 September 2011
Immune system with Serial Killers
An article from the New York Times. Very long but well worth a read. COOL STUFF!
An Immune System Trained to Kill Cancer
By DENISE GRADY
PHILADELPHIA — A year ago, when chemotherapy stopped working against his leukemia, William Ludwig signed up to be the first patient treated in a bold experiment at the University of Pennsylvania. Mr. Ludwig, then 65, a retired corrections officer from Bridgeton, N.J., felt his life draining away and thought he had nothing to lose.
Doctors removed a billion of his T-cells — a type of white blood cell that fights viruses and tumors — and gave them new genes that would program the cells to attack his cancer. Then the altered cells were dripped back into Mr. Ludwig’s veins.
At first, nothing happened. But after 10 days, hell broke loose in his hospital room. He began shaking with chills. His temperature shot up. His blood pressure shot down. He became so ill that doctors moved him into intensive care and warned that he might die. His family gathered at the hospital, fearing the worst.
A few weeks later, the fevers were gone. And so was the leukemia.There was no trace of it anywhere — no leukemic cells in his blood or bone marrow, no more bulging lymph nodes on his CT scan. His doctors calculated that the treatment had killed off two pounds of cancer cells.
A year later, Mr. Ludwig is still in complete remission. Before, there were days when he could barely get out of bed; now, he plays golf and does yard work. “I have my life back,” he said.
Mr. Ludwig’s doctors have not claimed that he is cured — it is too soon to tell — nor have they declared victory over leukemia on the basis of this experiment, which involved only three patients. The research, they say, has far to go; the treatment is still experimental, not available outside of studies.
But scientists say the treatment that helped Mr. Ludwig, described recently in The New England Journal of Medicine and Science Translational Medicine, may signify a turning point in the long struggle to develop effective gene therapies against cancer. And not just for leukemia patients: other cancers may also be vulnerable to this novel approach — which employs a disabled form of H.I.V.-1, the virus that causes AIDS, to carry cancer-fighting genes into the patients’ T-cells. In essence, the team is using gene therapy to accomplish something that researchers have hoped to do for decades: train a person’s own immune system to kill cancer cells.
Two other patients have undergone the experimental treatment. One had a partial remission: his disease lessened but did not go away completely. Another had a complete remission. All three had had advanced chronic lymphocytic leukemia and had run out of chemotherapy options. Usually, the only hope for a remission in such cases is a bone-marrow transplant, but these patients were not candidates for it.
Dr. Carl June, who led the research and directs translational medicine in the Abramson Cancer Center at the University of Pennsylvania, said that the results stunned even him and his colleagues, Dr. David L. Porter, Bruce Levine and Michael Kalos. They had hoped to see some benefit but had not dared dream of complete, prolonged remissions. Indeed, when Mr. Ludwig began running fevers, the doctors did not realize at first that it was a sign that his T-cells were engaged in a furious battle with his cancer.
Other experts in the field said the results were a major advance.“It’s great work,” said Dr. Walter J. Urba of the Providence Cancer Center and Earle A. Chiles Research Institute in Portland, Ore. He called the patients’ recoveries remarkable, exciting and significant. “I feel very positive about this new technology. Conceptually, it’s very, very big.”
Dr. Urba said he thought the approach would ultimately be used against other types of cancer as well as leukemia and lymphoma. But he cautioned, “For patients today, we’re not there yet.” And he added the usual scientific caveat: To be considered valid, the results must be repeated in more patients, and by other research teams.
Dr. June called the techniques “a harvest of the information from the molecular biology revolution over the past two decades.”
Hitting a Genetic Jackpot
To make T-cells search out and destroy cancer, researchers must equip them to do several tasks: recognize the cancer, attack it, multiply, and live on inside the patient. A number of research groups have been trying to do this, but the T-cells they engineered could not accomplish all the tasks. As a result, the cells’ ability to fight tumors has generally been temporary.
The University of Pennsylvania team seems to have hit all the targets at once. Inside the patients, the T-cells modified by the researchers multiplied to 1,000 to 10,000 times the number infused, wiped out the cancer and then gradually diminished, leaving a population of “memory” cells that can quickly proliferate again if needed.
The researchers said they were not sure which parts of their strategy made it work — special cell-culturing techniques, the use of H.I.V.-1 to carry new genes into the T-cells, or the particular pieces of DNA that they selected to reprogram the T-cells.
The concept of doctoring T-cells genetically was first developed in the 1980s by Dr. Zelig Eshhar at the Weizmann Institute of Science in Rehovot, Israel. It involves adding gene sequences from different sources to enable the T-cells to produce what researchers call chimeric antigen receptors, or CARs — protein complexes that transform the cells into, in Dr. June’s words, “serial killers.”
Mr. Ludwig’s disease, chronic lymphocytic leukemia is a cancer of B-cells, the part of the immune system that normally produces antibodies to fight infection. All B-cells, whether healthy or leukemic, have on their surfaces a protein called CD19. To treat patients with the disease, the researchers hoped to reprogram their T-cells to find CD19 and attack B-cells carrying it.
But which gene sequences should be used to reprogram the T-cells, from which sources? And how do you insert them?
Various research groups have used different methods. Viruses are often used as carriers (or vectors) to insert DNA into other cells because that kind of genetic sabotage is exactly what viruses normally specialize in doing. To modify their patients’ T-cells, Dr. June and his colleagues tried a daring approach: they used a disabled form of H.I.V.-1. They are the first ever to use H.I.V.-1 as the vector in gene therapy for cancer patients (the virus has been used in other diseases).
The AIDS virus is a natural for this kind of treatment, Dr. June said, because it evolved to invade T-cells. The idea of putting any form of the AIDS virus into people sounds a bit frightening, he acknowledged, but the virus used by his team was “gutted” and was no longer harmful. Other researchers had altered and disabled the virus by adding DNA from humans, mice and cows, and from a virus that infects woodchucks and another that infects cows. Each bit was chosen for a particular trait, all pieced together into a vector that Dr. June called a “Rube Goldberg-like solution” and “truly a zoo.”
“It incorporates the ability of H.I.V. to infect cells but not to reproduce itself,” he said.
To administer the treatment, the researchers collected as many of the patients’ T-cells as they could by passing their blood through a machine that removed the cells and returned the other blood components back into the patients’ veins. The T-cells were exposed to the vector, which transformed them genetically, and then were frozen. Meanwhile, the patients were given chemotherapy to deplete any remaining T-cells, because the native T-cells might impede the growth of the altered ones. Finally, the T-cells were infused back into the patients.
Then, Dr. June said, “The patient becomes a bioreactor” as the T-cells proliferate, pouring out chemicals called cytokines that cause fever, chills, fatigue and other flulike symptoms.
The treatment wiped out all of the patients’ B-cells, both healthy ones and leukemic ones, and will continue to do for as long as the new T-cells persist in the body, which could be forever (and ideally should be, to keep the leukemia at bay). The lack of B-cells means that the patients may be left vulnerable to infection, and they will need periodic infusions of a substance called intravenous immune globulin to protect them.
So far, the lack of B-cells has not caused problems for Mr. Ludwig. He receives the infusions every few months. He had been receiving them even before the experimental treatment because the leukemia had already knocked out his healthy B-cells.
One thing that is not clear is why Patient 1 and Patient 3 had complete remissions, and Patient 2 did not. The researchers said that when Patient 2 developed chills and fever, he was treated with steroids at another hospital, and the drugs may have halted the T-cells’ activity. But they cannot be sure. It may also be that his disease was too severe.
The researchers wrote an entire scientific article about Patient 3, which was published in The New England Journal of Medicine. Like the other patients, he also ran fevers and felt ill, but the reaction took longer to set in, and he also developed kidney and liver trouble — a sign of tumor lysis syndrome, a condition that occurs when large numbers of cancer cells die off and dump their contents, which can clog the kidneys. He was given drugs to prevent kidney damage. He had a complete remission.
What the journal article did not mention was that Patient 3 was almost not treated.
Because of his illness and some production problems, the researchers said, they could not produce anywhere near as many altered T-cells for him as they had for the other two patients — only 14 million (“a mouse dose,” Dr. Porter said), versus 1 billion for Mr. Ludwig and 580 million for Patient 2. After debate, they decided to treat him anyway.
Patient 3 declined to be interviewed, but he wrote anonymously about his experience for the University of Pennsylvania Web site. When he developed chills and a fever, he said, “I was sure the war was on — I was sure C.L.L. cells were dying.”
He wrote that he was a scientist, and that when he was young had dreamed of someday making a discovery that would benefit mankind. But, he concluded, “I never imagined I would be part of the experiment.”
When he told Patient 3 that he was remission, Dr. Porter said, they both had tears in their eyes.
Not Without Danger to Patients
While promising, the new techniques developed by the University of Pennsylvania researchers are not without danger to patients. Engineered T-cells have attacked healthy tissue in patients at other centers. Such a reaction killed a 39-year-old woman with advanced colon cancer in a study at the National Cancer Institute, researchers there reported last year in the journal Molecular Therapy.
She developed severe breathing trouble 15 minutes after receiving the T-cells, had to be put on a ventilator and died a few days later. Apparently, a protein target on the cancer cells was also present in her lungs, and the T-cells homed in on it.
Researchers at Memorial Sloan Kettering Cancer in New York also reported a death last year in a T-cell trial for leukemia (also published in Molecular Therapy). An autopsy found that the patient had apparently died from sepsis, not from the T-cells, but because he died just four days after the infusion, the researchers said they considered the treatment a possible factor.
Dr. June said his team hopes to use T-cells against solid tumors, including some that are very hard to treat, like mesothelioma and ovarian and pancreatic cancer. But possible adverse reactions are a real concern, he said, noting that one of the protein targets on the tumor cells is also found on membranes that line the chest and abdomen. T-cell attacks could cause serious inflammation in those membranes and mimic lupus, a serious autoimmune disease.
Even if the T-cells do not hit innocent targets, there are still risks. Proteins they release could cause a “cytokine storm”— high fevers, swelling, inflammation and dangerously low blood pressure — which can be fatal. Or, if the treatment rapidly kills billions of cancer cells, the debris can damage the kidney and cause other problems.
Even if the new T-cell treatment proves to work, the drug industry will be needed to mass produce it. But Dr. June said the research is being done only at universities, not at drug companies. For the drug industry to take interest, he said, there will have to be overwhelming proof that the treatment is far better than existing ones.
“Then I think they’ll jump into it,” he said. “My challenge now is to do this in a larger set of patients with randomization, and to show that we have the same effects.”
Mr. Ludwig said that when entered the trial, he had no options left. Indeed, Dr. June said that Mr. Ludwig was “almost dead” from the leukemia, and the effort to treat him was a “Hail Mary.”
Mr. Ludwig said: “I don’t recall anybody saying there was going to be a remission. I don’t think they were dreaming to that extent.”
The trial was a Phase 1 study, meaning that its main goal was to find out whether the treatment was safe, and at what dose. Of course, doctors and patients always hope that there will be some benefit, but that was not an official endpoint.
Mr. Ludwig thought that if the trial could buy him six months or a year, it would be worth the gamble. But even if the study did not help him, he felt it would still be worthwhile if he could help the study.
When the fevers hit, he had no idea that might be a good sign. Instead, he assumed the treatment was not working. But a few weeks later, he said that his oncologist, Dr. Alison Loren, told him, “We can’t find any cancer in your bone marrow.”
Remembering the moment, Mr. Ludwig paused and said, “I got goose bumps just telling you those words.”
“I feel wonderful,” Mr. Ludwig said during a recent interview. “I walked 18 holes on the golf course this morning.”
Before the study, he was weak, suffered repeated bouts of pneumonia and was wasting away. Now, he is full of energy. He has gained 40 pounds. He and his wife bought an R.V., in which they travel with their grandson and nephew. “I feel normal, like I did 10 years before I was diagnosed,” Mr. Ludwig said. “This clinical trial saved my life.”
Dr. Loren said in an interview, “I hate to say it in that dramatic way, but I do think it saved his life.”
Mr. Ludwig said that Dr. Loren told him and his wife something he considered profound. “She said, ‘We don’t know how long it’s going to last. Enjoy every day,’ ” Mr. Ludwig recalled.
“That’s what we’ve done ever since.”
Doctors removed a billion of his T-cells — a type of white blood cell that fights viruses and tumors — and gave them new genes that would program the cells to attack his cancer. Then the altered cells were dripped back into Mr. Ludwig’s veins.
At first, nothing happened. But after 10 days, hell broke loose in his hospital room. He began shaking with chills. His temperature shot up. His blood pressure shot down. He became so ill that doctors moved him into intensive care and warned that he might die. His family gathered at the hospital, fearing the worst.
A few weeks later, the fevers were gone. And so was the leukemia.There was no trace of it anywhere — no leukemic cells in his blood or bone marrow, no more bulging lymph nodes on his CT scan. His doctors calculated that the treatment had killed off two pounds of cancer cells.
A year later, Mr. Ludwig is still in complete remission. Before, there were days when he could barely get out of bed; now, he plays golf and does yard work. “I have my life back,” he said.
Mr. Ludwig’s doctors have not claimed that he is cured — it is too soon to tell — nor have they declared victory over leukemia on the basis of this experiment, which involved only three patients. The research, they say, has far to go; the treatment is still experimental, not available outside of studies.
But scientists say the treatment that helped Mr. Ludwig, described recently in The New England Journal of Medicine and Science Translational Medicine, may signify a turning point in the long struggle to develop effective gene therapies against cancer. And not just for leukemia patients: other cancers may also be vulnerable to this novel approach — which employs a disabled form of H.I.V.-1, the virus that causes AIDS, to carry cancer-fighting genes into the patients’ T-cells. In essence, the team is using gene therapy to accomplish something that researchers have hoped to do for decades: train a person’s own immune system to kill cancer cells.
Two other patients have undergone the experimental treatment. One had a partial remission: his disease lessened but did not go away completely. Another had a complete remission. All three had had advanced chronic lymphocytic leukemia and had run out of chemotherapy options. Usually, the only hope for a remission in such cases is a bone-marrow transplant, but these patients were not candidates for it.
Dr. Carl June, who led the research and directs translational medicine in the Abramson Cancer Center at the University of Pennsylvania, said that the results stunned even him and his colleagues, Dr. David L. Porter, Bruce Levine and Michael Kalos. They had hoped to see some benefit but had not dared dream of complete, prolonged remissions. Indeed, when Mr. Ludwig began running fevers, the doctors did not realize at first that it was a sign that his T-cells were engaged in a furious battle with his cancer.
Other experts in the field said the results were a major advance.“It’s great work,” said Dr. Walter J. Urba of the Providence Cancer Center and Earle A. Chiles Research Institute in Portland, Ore. He called the patients’ recoveries remarkable, exciting and significant. “I feel very positive about this new technology. Conceptually, it’s very, very big.”
Dr. Urba said he thought the approach would ultimately be used against other types of cancer as well as leukemia and lymphoma. But he cautioned, “For patients today, we’re not there yet.” And he added the usual scientific caveat: To be considered valid, the results must be repeated in more patients, and by other research teams.
Dr. June called the techniques “a harvest of the information from the molecular biology revolution over the past two decades.”
Hitting a Genetic Jackpot
To make T-cells search out and destroy cancer, researchers must equip them to do several tasks: recognize the cancer, attack it, multiply, and live on inside the patient. A number of research groups have been trying to do this, but the T-cells they engineered could not accomplish all the tasks. As a result, the cells’ ability to fight tumors has generally been temporary.
The University of Pennsylvania team seems to have hit all the targets at once. Inside the patients, the T-cells modified by the researchers multiplied to 1,000 to 10,000 times the number infused, wiped out the cancer and then gradually diminished, leaving a population of “memory” cells that can quickly proliferate again if needed.
The researchers said they were not sure which parts of their strategy made it work — special cell-culturing techniques, the use of H.I.V.-1 to carry new genes into the T-cells, or the particular pieces of DNA that they selected to reprogram the T-cells.
The concept of doctoring T-cells genetically was first developed in the 1980s by Dr. Zelig Eshhar at the Weizmann Institute of Science in Rehovot, Israel. It involves adding gene sequences from different sources to enable the T-cells to produce what researchers call chimeric antigen receptors, or CARs — protein complexes that transform the cells into, in Dr. June’s words, “serial killers.”
Mr. Ludwig’s disease, chronic lymphocytic leukemia is a cancer of B-cells, the part of the immune system that normally produces antibodies to fight infection. All B-cells, whether healthy or leukemic, have on their surfaces a protein called CD19. To treat patients with the disease, the researchers hoped to reprogram their T-cells to find CD19 and attack B-cells carrying it.
But which gene sequences should be used to reprogram the T-cells, from which sources? And how do you insert them?
Various research groups have used different methods. Viruses are often used as carriers (or vectors) to insert DNA into other cells because that kind of genetic sabotage is exactly what viruses normally specialize in doing. To modify their patients’ T-cells, Dr. June and his colleagues tried a daring approach: they used a disabled form of H.I.V.-1. They are the first ever to use H.I.V.-1 as the vector in gene therapy for cancer patients (the virus has been used in other diseases).
The AIDS virus is a natural for this kind of treatment, Dr. June said, because it evolved to invade T-cells. The idea of putting any form of the AIDS virus into people sounds a bit frightening, he acknowledged, but the virus used by his team was “gutted” and was no longer harmful. Other researchers had altered and disabled the virus by adding DNA from humans, mice and cows, and from a virus that infects woodchucks and another that infects cows. Each bit was chosen for a particular trait, all pieced together into a vector that Dr. June called a “Rube Goldberg-like solution” and “truly a zoo.”
“It incorporates the ability of H.I.V. to infect cells but not to reproduce itself,” he said.
To administer the treatment, the researchers collected as many of the patients’ T-cells as they could by passing their blood through a machine that removed the cells and returned the other blood components back into the patients’ veins. The T-cells were exposed to the vector, which transformed them genetically, and then were frozen. Meanwhile, the patients were given chemotherapy to deplete any remaining T-cells, because the native T-cells might impede the growth of the altered ones. Finally, the T-cells were infused back into the patients.
Then, Dr. June said, “The patient becomes a bioreactor” as the T-cells proliferate, pouring out chemicals called cytokines that cause fever, chills, fatigue and other flulike symptoms.
The treatment wiped out all of the patients’ B-cells, both healthy ones and leukemic ones, and will continue to do for as long as the new T-cells persist in the body, which could be forever (and ideally should be, to keep the leukemia at bay). The lack of B-cells means that the patients may be left vulnerable to infection, and they will need periodic infusions of a substance called intravenous immune globulin to protect them.
So far, the lack of B-cells has not caused problems for Mr. Ludwig. He receives the infusions every few months. He had been receiving them even before the experimental treatment because the leukemia had already knocked out his healthy B-cells.
One thing that is not clear is why Patient 1 and Patient 3 had complete remissions, and Patient 2 did not. The researchers said that when Patient 2 developed chills and fever, he was treated with steroids at another hospital, and the drugs may have halted the T-cells’ activity. But they cannot be sure. It may also be that his disease was too severe.
The researchers wrote an entire scientific article about Patient 3, which was published in The New England Journal of Medicine. Like the other patients, he also ran fevers and felt ill, but the reaction took longer to set in, and he also developed kidney and liver trouble — a sign of tumor lysis syndrome, a condition that occurs when large numbers of cancer cells die off and dump their contents, which can clog the kidneys. He was given drugs to prevent kidney damage. He had a complete remission.
What the journal article did not mention was that Patient 3 was almost not treated.
Because of his illness and some production problems, the researchers said, they could not produce anywhere near as many altered T-cells for him as they had for the other two patients — only 14 million (“a mouse dose,” Dr. Porter said), versus 1 billion for Mr. Ludwig and 580 million for Patient 2. After debate, they decided to treat him anyway.
Patient 3 declined to be interviewed, but he wrote anonymously about his experience for the University of Pennsylvania Web site. When he developed chills and a fever, he said, “I was sure the war was on — I was sure C.L.L. cells were dying.”
He wrote that he was a scientist, and that when he was young had dreamed of someday making a discovery that would benefit mankind. But, he concluded, “I never imagined I would be part of the experiment.”
When he told Patient 3 that he was remission, Dr. Porter said, they both had tears in their eyes.
Not Without Danger to Patients
While promising, the new techniques developed by the University of Pennsylvania researchers are not without danger to patients. Engineered T-cells have attacked healthy tissue in patients at other centers. Such a reaction killed a 39-year-old woman with advanced colon cancer in a study at the National Cancer Institute, researchers there reported last year in the journal Molecular Therapy.
She developed severe breathing trouble 15 minutes after receiving the T-cells, had to be put on a ventilator and died a few days later. Apparently, a protein target on the cancer cells was also present in her lungs, and the T-cells homed in on it.
Researchers at Memorial Sloan Kettering Cancer in New York also reported a death last year in a T-cell trial for leukemia (also published in Molecular Therapy). An autopsy found that the patient had apparently died from sepsis, not from the T-cells, but because he died just four days after the infusion, the researchers said they considered the treatment a possible factor.
Dr. June said his team hopes to use T-cells against solid tumors, including some that are very hard to treat, like mesothelioma and ovarian and pancreatic cancer. But possible adverse reactions are a real concern, he said, noting that one of the protein targets on the tumor cells is also found on membranes that line the chest and abdomen. T-cell attacks could cause serious inflammation in those membranes and mimic lupus, a serious autoimmune disease.
Even if the T-cells do not hit innocent targets, there are still risks. Proteins they release could cause a “cytokine storm”— high fevers, swelling, inflammation and dangerously low blood pressure — which can be fatal. Or, if the treatment rapidly kills billions of cancer cells, the debris can damage the kidney and cause other problems.
Even if the new T-cell treatment proves to work, the drug industry will be needed to mass produce it. But Dr. June said the research is being done only at universities, not at drug companies. For the drug industry to take interest, he said, there will have to be overwhelming proof that the treatment is far better than existing ones.
“Then I think they’ll jump into it,” he said. “My challenge now is to do this in a larger set of patients with randomization, and to show that we have the same effects.”
Mr. Ludwig said that when entered the trial, he had no options left. Indeed, Dr. June said that Mr. Ludwig was “almost dead” from the leukemia, and the effort to treat him was a “Hail Mary.”
Mr. Ludwig said: “I don’t recall anybody saying there was going to be a remission. I don’t think they were dreaming to that extent.”
The trial was a Phase 1 study, meaning that its main goal was to find out whether the treatment was safe, and at what dose. Of course, doctors and patients always hope that there will be some benefit, but that was not an official endpoint.
Mr. Ludwig thought that if the trial could buy him six months or a year, it would be worth the gamble. But even if the study did not help him, he felt it would still be worthwhile if he could help the study.
When the fevers hit, he had no idea that might be a good sign. Instead, he assumed the treatment was not working. But a few weeks later, he said that his oncologist, Dr. Alison Loren, told him, “We can’t find any cancer in your bone marrow.”
Remembering the moment, Mr. Ludwig paused and said, “I got goose bumps just telling you those words.”
“I feel wonderful,” Mr. Ludwig said during a recent interview. “I walked 18 holes on the golf course this morning.”
Before the study, he was weak, suffered repeated bouts of pneumonia and was wasting away. Now, he is full of energy. He has gained 40 pounds. He and his wife bought an R.V., in which they travel with their grandson and nephew. “I feel normal, like I did 10 years before I was diagnosed,” Mr. Ludwig said. “This clinical trial saved my life.”
Dr. Loren said in an interview, “I hate to say it in that dramatic way, but I do think it saved his life.”
Mr. Ludwig said that Dr. Loren told him and his wife something he considered profound. “She said, ‘We don’t know how long it’s going to last. Enjoy every day,’ ” Mr. Ludwig recalled.
“That’s what we’ve done ever since.”
Monday, 5 September 2011
Endurance exercise encourages stem cells to make bone instead of fat
Mesenchymal stem cells are a type of adult stem cells found throughout the body. These cells can form fat, bone or cartilage cells.
Researchers in Canada found that endurance exercise encourages mesenchymal stem cells to become bone instead of fat cells.
In this study, one group of mice were trained on a treadmill at progressive speeds over a 10-week period. While the other group was made to simply watch life go by. Tissues were harvested 2 days following the final training session.
Results of this study show that:
This could be true in humans too... so.. HIT THE GYM PEOPLE!
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| Source: http://www.chumpysclipart.com |
Friday, 2 September 2011
Fat cells help hair to grow
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| Manchester United Striker Wayne Rooney had a hair transplant to combat his receding hairline |
With all that $kaching$ and fame and prowess on the field, who would have thought that Rooney concerns himself over hair! But yes, having more hair certainly makes one feel more confident. Man U won 8-2 against arsenal in a league game. Hello?!?!
Up close with your hair
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| Illustration of how it looks like at the root of a strand of hair. Source: hairrestorationadvice.com |
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| Hair Growth Cycle. Source: womentowomen.com |
Fat cells secrete chemicals that helps hair grow
According to a report on BBC news, fat cells in the skin have been identified as the source of chemicals needed to make hair grow.
Their work, published in the journal Cell, showed that:
1) Defective mice which could not produce fat cells. The hair follicles had become trapped in the dormant phase of the hair cycle.
2) When fat cells from healthy mice were injected into defective mice, hair follicles started to grow after 2 weeks.
3) Precursor fat cells produce a chemical - a platelet-derived growth factor (PDGF) - at 100 times the level of surrounding cells.
4) Injecting PDGF into the skin of defective mice kicks-start growth in 86% of follicles.
It'll be interesting to see if PDGF affects hair growth in humans, or if other factors secreted by these precursor fat cells can help stimulate hair growth. I look forward to further great work from the lab of Prof Horsley!
Hmm... I have a few tubes of PDGF in the lab... tempting.... ;P
Thursday, 1 September 2011
UK stem cell stroke trial passes first safety test
Article from BBC news:
The assessment paves the way for the therapy to be tested on more patients to find a new treatment for stroke.
The hope is that the stem cells will help to repair damaged brain tissue.
The trial is being led by Prof Keith Muir of Glasgow University. He told BBC News that he was pleased with the results so far.
"We need to be assured of safety before we can progress to trying to test the effects of this therapy. Because this is the first time this type of cell therapy has been used in humans, it's vitally important that we determine that it's safe to proceed - so at the present time we have the clearance to proceed to the next higher dose of cells."
An elderly man was the first person in the world to receive this treatment last year. Since then it has been tried out on two more patients.
Global trials
The patients have received very low doses of stem cells in trials designed to test the safety of the procedure.
The development of stem cell treatments is still at an early stage and it is likely to be many years before these treatments become widely available.
Strokes kill about 67,000 people in the UK every year, according to the Stroke Association.
The charity says it is the third most common cause of death in England and Wales after heart disease and cancer.
The stroke trial is being carried out with Reneuron Group plc. The company's chief executive officer Michael Hunt said there was a long way to go.
"The earliest a treatment could be widely available if everything goes very well is five years. It is very much a case of so far, so good. It is still at a very early stage but we draw great comfort from these results."
The world's first clinical trial of brain stem cells to treat strokes is set to move to its next phase.
An independent assessment of the first three patients to have had stem cells injected into their brain at Glasgow's Southern General Hospital has concluded it has had no adverse effect.The assessment paves the way for the therapy to be tested on more patients to find a new treatment for stroke.
The hope is that the stem cells will help to repair damaged brain tissue.
The trial is being led by Prof Keith Muir of Glasgow University. He told BBC News that he was pleased with the results so far.
"We need to be assured of safety before we can progress to trying to test the effects of this therapy. Because this is the first time this type of cell therapy has been used in humans, it's vitally important that we determine that it's safe to proceed - so at the present time we have the clearance to proceed to the next higher dose of cells."
An elderly man was the first person in the world to receive this treatment last year. Since then it has been tried out on two more patients.
Global trials
The patients have received very low doses of stem cells in trials designed to test the safety of the procedure.
Over the next year, up to nine more patients will be given progressively higher doses - again primarily to assess safety - but doctors will also be using this clinical trial to assess the best ways of measuring the effectiveness of the treatment in subsequent larger trials, which would not begin for at least 18 months.
There are a growing number of well-regulated clinical trials of stem cell treatments now under way in various parts of the world, including one which also began last year by the US firm Geron to develop a treatment for paralysis. The development of stem cell treatments is still at an early stage and it is likely to be many years before these treatments become widely available.
Strokes kill about 67,000 people in the UK every year, according to the Stroke Association.
The charity says it is the third most common cause of death in England and Wales after heart disease and cancer.
The stroke trial is being carried out with Reneuron Group plc. The company's chief executive officer Michael Hunt said there was a long way to go.
"The earliest a treatment could be widely available if everything goes very well is five years. It is very much a case of so far, so good. It is still at a very early stage but we draw great comfort from these results."
Wednesday, 31 August 2011
Bad sleep ups blood pressure risk
On BBC news:
Elderly men who spend little time in deep sleep could be at risk of developing high blood pressure, according to US scientists.
The British Heart Foundation said it was important for everyone to prioritise sleep.
High blood pressure - also known as hypertension - increases the risk of heart attack, stroke and other health problems.
Researchers measured the "sleep quality" of 784 men over the age of 65 between 2007 and 2009. At the start none had hypertension, while 243 had the condition by the end of the study.
The patients were split into groups based on the percentage of time asleep spent in deep, or slow wave, sleep. Those in the lowest group - 4% deep sleep - had a 1.83-fold increased risk of hypertension compared with those in the highest group, who spent 17% of the night in deep sleep.
One of the report's authors, Professor Susan Redline from Harvard Medical School, said: "Our study shows for the first time that poor quality sleep, reflected by reduced slow wave sleep, puts individuals at significantly increased risk of developing high blood pressure.
The report said further studies were needed to determine if improving sleep could reduce the risk.
Natasha Stewart, senior cardiac nurse at the British Heart Foundation, said: "Whilst this study does suggest a link between lack of sleep and the development of high blood pressure, it only looked at men aged over 65.
"We would need to see more research in other age groups and involving women to confirm this particular association.
"However, we do know more generally that sleep is essential for staying healthy. It's important we all try to make sleep a priority and get our six to eight hours of shut-eye a night."
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| Sleeping Beauty |
Sunday, 28 August 2011
Are males necessary?
A recent article published on National Geographic talked about an insect species, known as cottony cushion scale, where females have begun to develop sperm-producing clones of their fathers—inside their bodies.
When baby girl cushion scales develop in the mother’s fertilized eggs, excess sperm from the father grows into tissue within her body. This tissue is genetically identical to the father. The “father’s sperms” lives inside the female and fertilize her eggs internally—rendering the female a hermaphrodite and making her father both the grandfather and father of her offspring.
Though this new form of reproduction hasn't replaced cottony cushion scale sex, "this parasitic male has taken off like an epidemic in population," said study leader Andy Gardner, an evolutionary theorist at the University of Oxford.
"Once [this trend] gets started, it's going to sweep through the population so all the females carry it. So there's no point for regular males to exist," Gardner added.
If the females begin passing on the parasitic male to their offspring, there may eventually be no more need for "baby boy" cushion scales that grow up and produce sperm and fertilize females, Gardner said.
This work, published in the August issue of American Naturalist, suggests that the females would benefit from this parasitic infection, negating the need for males.
WOW! That’s pretty interesting. Although I don’t think it will benefit the species in the long term. Sexual reproduction introduces genetic variation in the offsprings. This makes the population better able to keep up with changes in the environment. Asexual reproduction produces a genetically similar population, which may all be easily wiped out by the same disease.
When baby girl cushion scales develop in the mother’s fertilized eggs, excess sperm from the father grows into tissue within her body. This tissue is genetically identical to the father. The “father’s sperms” lives inside the female and fertilize her eggs internally—rendering the female a hermaphrodite and making her father both the grandfather and father of her offspring.
 |
| Cottony Cushion Scale |
Though this new form of reproduction hasn't replaced cottony cushion scale sex, "this parasitic male has taken off like an epidemic in population," said study leader Andy Gardner, an evolutionary theorist at the University of Oxford.
"Once [this trend] gets started, it's going to sweep through the population so all the females carry it. So there's no point for regular males to exist," Gardner added.
If the females begin passing on the parasitic male to their offspring, there may eventually be no more need for "baby boy" cushion scales that grow up and produce sperm and fertilize females, Gardner said.
This work, published in the August issue of American Naturalist, suggests that the females would benefit from this parasitic infection, negating the need for males.
WOW! That’s pretty interesting. Although I don’t think it will benefit the species in the long term. Sexual reproduction introduces genetic variation in the offsprings. This makes the population better able to keep up with changes in the environment. Asexual reproduction produces a genetically similar population, which may all be easily wiped out by the same disease.
Furthermore, what’s the fun in reproducing if deprived of the joy of the mating process?:D
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| Hermaphroditus, the two-sexed son of Aphrodite and Hermes, was portrayed in Greco-Roman art as a female figure with male genitals. Hermaphroditus is a symbol of bisexuality or effeminacy, |
Sunday, 21 August 2011
very long but MUST READ entry
A news article from Boston.com
NEW YORK - He calls it innovative. Others call it a big risk. In any case, the stem cell procedure that Governor Rick Perry of Texas had last month was an unapproved experimental way of fixing a common malady: a bad back.
Perry, the newest GOP presidential candidate, has access to the best possible care. Yet he and his doctor chose a treatment beyond mainstream medicine: He had stem cells taken from fat in his own body, grown in a lab, and then injected into his back and his bloodstream during a July 1 operation to fuse part of his spine.
The treatment carries potential risks ranging from blood clots to cancer and may run afoul of federal rules, doctors say. At least one patient died of a clot hours after an infusion of fat-derived stem cells outside the United States. It is not clear how much of this Perry might have known.
His doctor and friend, orthopedist Stanley Jones, could not be reached for comment despite repeated requests to the spokeswoman for his Houston-area hospital. Jones told the Texas Tribune that he went to Japan for a stem cell treatment that helped his arthritis and that he had never before tried the procedure he used on Perry. He also said it had no risks.
However, some scientists are questioning the safety and wisdom of Perry’s treatment, especially because it was not part of a clinical trial in which unproven therapies are tested in a way that helps protect patients and advances medical knowledge.
Perry “exercised poor judgment’’ to try it, said Dr. George Q. Daley of Children’s Hospital Boston and the Harvard Stem Cell Institute. “As a highly influential person of power, Perry’s actions have the unfortunate potential to push desperate patients into the clinics of quacks’’ who are selling unproven treatments “for everything from Alzheimer’s to autism.’’
Daley is past president of the International Society for Stem Cell Research, a group of 3,000 scientists and others in the field. He favors stem cell research. But of Perry’s treatment he said: “I would never in a million years accept for one of my family members to undergo this.’’
On the campaign trail Thursday in New Hampshire, Ray Sullivan, Perry’s chief of staff, said: “The governor consulted with his physician and decided the best course of action for him. He’s very pleased with the results of the surgery, with the rapid recovery, and with the procedure that he had.’’
Perry’s treatment was first reported by the Texas Tribune. The procedure was done by Jones, who works at Foundation Surgical Hospital, but Perry spokesman Mark Miner would not say where it took place.
It used Perry’s own “adult’’ stem cells - not embryonic stem cells, a controversial technology that involves destroying an embryo, which the governor opposes. Adult stem cells have long been used to treat cancers such as leukemia and lymphoma - they are what doctors use it bone marrow transplants. The cells are being studied for everything from heart disease to diabetes, but it is too soon to know if these approaches are safe or effective.
Some orthopedic surgeons are experimenting with stem cells to help bones heal. The cells usually are taken from bone marrow and injected or implanted in the trouble spot, such as a knee or shoulder. The theory is that these “master cells’’ will follow cues from cells around them and form bone or cartilage, though scientists worry they also might spur unwanted growth and cancer.
Perry, however, had an even more experimental procedure: stem cells from fat removed by liposuction and grown in a lab before they were put into his spine and bloodstream.
Dr. George Muschler, an orthopedic surgeon at Cleveland Clinic, said fat-derived stem cells are “an unusual choice’’ because they do not form bone as readily.
Using them as was done for Perry is “quite experimental and it’s quite controversial because there isn’t good evidence yet, at least in the medical literature, that fat cells work better or even work at all in repairing bones,’’ said Muschler, who has developed three patents on cell-related technologies.
Dr. Thomas Einhorn, orthopedics chairman at Boston University, has tested experimental stem cell therapies. He said one concern is that Perry’s cells were grown in a lab dish with other ingredients, where there is more of a risk they will transform into cancer and any breach in sterility could lead to an infection.
He also took issue with infusing the cells into Perry’s bloodstream. “I can’t think of any reason to do that. I wouldn’t want to cause a blood clot.’’
It also enters a gray area with the FDA, which does not regulate how doctors practice medicine but does oversee medical products. Growing the cells in culture and possibly mixing them with other substances may make these modified cells a product. FDA spokeswoman Shelly Burgess said the agency could not comment on Perry’s treatment.
Oh dear. This sounds like suicide to me. Or a conspiracy theory to thwart the public's trust in stem cell research. Or, just PLAIN STUPIDITY.
NEW YORK - He calls it innovative. Others call it a big risk. In any case, the stem cell procedure that Governor Rick Perry of Texas had last month was an unapproved experimental way of fixing a common malady: a bad back.
Perry, the newest GOP presidential candidate, has access to the best possible care. Yet he and his doctor chose a treatment beyond mainstream medicine: He had stem cells taken from fat in his own body, grown in a lab, and then injected into his back and his bloodstream during a July 1 operation to fuse part of his spine.
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| Gov Rick Perry |
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| Dr Stanley Jones |
However, some scientists are questioning the safety and wisdom of Perry’s treatment, especially because it was not part of a clinical trial in which unproven therapies are tested in a way that helps protect patients and advances medical knowledge.
Perry “exercised poor judgment’’ to try it, said Dr. George Q. Daley of Children’s Hospital Boston and the Harvard Stem Cell Institute. “As a highly influential person of power, Perry’s actions have the unfortunate potential to push desperate patients into the clinics of quacks’’ who are selling unproven treatments “for everything from Alzheimer’s to autism.’’
Daley is past president of the International Society for Stem Cell Research, a group of 3,000 scientists and others in the field. He favors stem cell research. But of Perry’s treatment he said: “I would never in a million years accept for one of my family members to undergo this.’’
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| Dr George Daley |
On the campaign trail Thursday in New Hampshire, Ray Sullivan, Perry’s chief of staff, said: “The governor consulted with his physician and decided the best course of action for him. He’s very pleased with the results of the surgery, with the rapid recovery, and with the procedure that he had.’’
Perry’s treatment was first reported by the Texas Tribune. The procedure was done by Jones, who works at Foundation Surgical Hospital, but Perry spokesman Mark Miner would not say where it took place.
It used Perry’s own “adult’’ stem cells - not embryonic stem cells, a controversial technology that involves destroying an embryo, which the governor opposes. Adult stem cells have long been used to treat cancers such as leukemia and lymphoma - they are what doctors use it bone marrow transplants. The cells are being studied for everything from heart disease to diabetes, but it is too soon to know if these approaches are safe or effective.
Some orthopedic surgeons are experimenting with stem cells to help bones heal. The cells usually are taken from bone marrow and injected or implanted in the trouble spot, such as a knee or shoulder. The theory is that these “master cells’’ will follow cues from cells around them and form bone or cartilage, though scientists worry they also might spur unwanted growth and cancer.
Dr. George Muschler, an orthopedic surgeon at Cleveland Clinic, said fat-derived stem cells are “an unusual choice’’ because they do not form bone as readily.
Using them as was done for Perry is “quite experimental and it’s quite controversial because there isn’t good evidence yet, at least in the medical literature, that fat cells work better or even work at all in repairing bones,’’ said Muschler, who has developed three patents on cell-related technologies.
Dr. Thomas Einhorn, orthopedics chairman at Boston University, has tested experimental stem cell therapies. He said one concern is that Perry’s cells were grown in a lab dish with other ingredients, where there is more of a risk they will transform into cancer and any breach in sterility could lead to an infection.
He also took issue with infusing the cells into Perry’s bloodstream. “I can’t think of any reason to do that. I wouldn’t want to cause a blood clot.’’
It also enters a gray area with the FDA, which does not regulate how doctors practice medicine but does oversee medical products. Growing the cells in culture and possibly mixing them with other substances may make these modified cells a product. FDA spokeswoman Shelly Burgess said the agency could not comment on Perry’s treatment.
Oh dear. This sounds like suicide to me. Or a conspiracy theory to thwart the public's trust in stem cell research. Or, just PLAIN STUPIDITY.
Nose
Everyone knows that people who live in cold countries like Siberia and Greenland have narrower and longer noses compared to those of us who live in countries like Singapore with hot humid climate.
A recent study by researchers in Germany explained why individuals from cold, dry climates had higher and narrower nasal cavities than those from hot, humid climates.
Narrow nasal passage enhances contact between the air and mucus in the nose, which helps to warm and humidify the air. People in cold climate have more space in the nose to warm up the incoming air.
Moreover, microscopic hairs called cilia, which line the nasal passage, help to keep out pathogens and dust that may infect or irritate the lungs, and the cilia work more efficiently when incoming air is moist. This explains why people from warm climates, moving into cold climates, could be more susceptible to nasal irritation, colds and other sinus-related problems.
Source: http://www.scientificamerican.com/article.cfm?id=the-shape-of-a-nose
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| Miss Siberia 2009 |
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| Miss Singapore 2009 |
A recent study by researchers in Germany explained why individuals from cold, dry climates had higher and narrower nasal cavities than those from hot, humid climates.
Narrow nasal passage enhances contact between the air and mucus in the nose, which helps to warm and humidify the air. People in cold climate have more space in the nose to warm up the incoming air.
Moreover, microscopic hairs called cilia, which line the nasal passage, help to keep out pathogens and dust that may infect or irritate the lungs, and the cilia work more efficiently when incoming air is moist. This explains why people from warm climates, moving into cold climates, could be more susceptible to nasal irritation, colds and other sinus-related problems.
Source: http://www.scientificamerican.com/article.cfm?id=the-shape-of-a-nose
Tuesday, 16 August 2011
Faithful gay birds
A study carried out by Julie Elie and colleagues at the UC-Berkeley found that zebra finches form same-sex monogamous relationships and are just as attached and faithful to each other as those paired with a member of the opposite sex.
When raised in male-only groups, more than half of the birds paired up in same-sex couplings. The birds first displayed courtship behavior by singing and preening each other. When bonded, they perch side by side, nestled together and greet each other by "nuzzling" beaks.
Interestingly, when females were introduced to the groups, five out of eight stuck with their gay partners and ignored the female.
“The findings indicate that, even in birds, the drive to find a mate is far more complicated than simply the need to reproduce. A pair-bond in socially monogamous species represents a cooperative partnership that may give advantages for survival," said Dr Elie. "Finding a social partner, whatever its sex, could be a priority."
Sunday, 14 August 2011
We heart stem cells
Recently, an article entitled "A*Star scientists closer to growing human heart from stem cells" was published in the Straits Times.
In this paper, researchers from the Institute of Bioengineering and Nanotechnology
1) Decellularized mouse heart: i.e. removed the cells from the mouse heart, leaving only the scaffold
2) Seeded the scaffold with human embryonic stem cells (hESCs) and heart progenitors derived from hESC
3) Implanted the heart back into the mouse
They found that the cells attached to the scaffold and developed into heart cells and blood vessel cells, both important for proper functioning of the heart.
However, this discovery is not entirely novel. In 2008, researchers from University of Minnesota already showed that the scaffold from decellularized heart supports development of heart progenitors into an adult heart.
Read the news release here.
Novel or not, both studies deserve the spotlight as they remind us that building an organ with stem cells may not be that far-fetched an idea after all.
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| Satirical cartoon of China harvesting organs from Falun Gong prisoners. Source: http://nicholsoncartoons.com.au/falun-gong-organ-harvesting-china-550.html |
Thursday, 11 August 2011
Let there be aliens
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| Image from space by astronaut photographer. Source: Time Lightbox Photo Essay by Phil Bicker |
According to Dr Michael Callahan, who published this finding in Proceedings of the National Academy of Sciences, "Hydrogen cyanide, ammonia and water exist throughout the cosmos. When mixed together, they could make nucleobases."
Tuesday, 9 August 2011
Thursday, 4 August 2011
10 years of science scholarship
Today, the Agency for Science, Technology and Research (A*STAR) celebrates its 10th year of giving out scholarships to young Singaporeans.
I felt rather nostalgic looking at these young scholars receiving their awards.
10 years ago, I received the A*STAR National Science Scholarship, which paid for
1) My undergraduate studies in the US
and
2) PhD studies in the UK
And now I am back in Singapore serving out THE BOND.
Of course, there have been times when I doubted my decision to take up the scholarship. Hey, I was only 19 when I signed my life away! But as the saying goes, "the grass is not always greener on the other side, but greener where you water it".
This scholarship gave me the chance to study at top universities, let me spend the prime of my youth overseas, and took care of me financially. Importantly, I have an interesting job now and am optimistic about future career prospects.
For all of that, I thank A*STAR (and Singapore taxpayers' money!) for helping me get to where I am today.
So, thank you, and happy 10th anniversary.
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| Guest of honor: Minister for Education Mr Heng Swee Keat giving his speech |
10 years ago, I received the A*STAR National Science Scholarship, which paid for
1) My undergraduate studies in the US
 |
| Freshman year bonfire! |
2) PhD studies in the UK
 |
| Rowing for Cambridge May Bumps |
Of course, there have been times when I doubted my decision to take up the scholarship. Hey, I was only 19 when I signed my life away! But as the saying goes, "the grass is not always greener on the other side, but greener where you water it".
This scholarship gave me the chance to study at top universities, let me spend the prime of my youth overseas, and took care of me financially. Importantly, I have an interesting job now and am optimistic about future career prospects.
For all of that, I thank A*STAR (and Singapore taxpayers' money!) for helping me get to where I am today.
So, thank you, and happy 10th anniversary.
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