Onions are one of the richest sources of sulfur-containing compounds which have been shown to slow down the deterioration of memory.

People suffering from memory loss who ate the layered vegetable found it improved their ability to recall, researchers at Hokkaido Tokai University in Japan said.
Experts said the findings could be important in the fight against brain diseases such as Alzheimer’s and Parkinson’s, Independent.ie reported.
The researchers discovered an antioxidant found in onions binds with harmful toxins in the brain and flushes them out of the body.
The compound, which contains sulfur, is found in many members of the allum family, including garlic.
Food expert Ian Marber said: “Onions are one of the richest and most readily available sources of sulfur-containing compounds which have been shown to slow down the deterioration of memory usually associated with ageing.
“Onion extract has also been shown to maintain the hippocampus, a part of the brain that is involved in processing emotions as well as memory.’’
But he warned onions that are over-cooked may lose their memory-helping properties. They should instead be cooked on a low heat.
The research compounds onions’ reputation as being good for your memory.
A recent French study found a high flavonoid intake can reduce memory loss associated with ageing. Onions contain a flavonoid called quercetin, and in greater quantities than in tea and apples.
Other evidence credits onions with success at combating the common cold, hayfever and heart disease.

The foreground object is the planet-mass object. The pulsar, located at the upper right, is tidally distorting the companion into a teardrop-shaped object, and ripping gas from it.

Using NASA’s Swift and Rossi X-ray Timing Explorer (RXTE) satellites, astronomers have discovered one of the most bizarre planet-mass objects ever found. The object’s minimum mass is only about 7 times the mass of Jupiter. But instead of orbiting a normal star, this low-mass body orbits a rapidly spinning pulsar. It orbits the pulsar every 54.7 minutes at an average distance of only about 230,000 miles (slightly less than the Earth-Moon distance).
“This object is merely the skeleton of a star,“ says co-discoverer Craig Markwardt of NASA’s Goddard Space Flight Center in Greenbelt, Md. “The pulsar has eaten away the star’s outer envelope, and all the remains is its helium-rich core.“
Hans Krimm of NASA Goddard discovered the system on June 7, when Swift’s Burst Alert Telescope picked up an outburst of X rays and gamma rays in the direction of the galactic center. The source was named SWIFT J1756.9-2508 for its sky coordinates in the constellation Sagittarius, Astronomy.com said.
RXTE began observing SWIFT J1756.9 on June 13 with its Proportional Counter Array (PCA). After analyzing the PCA data, Markwardt realized that the object was pulsing in X rays 182.07 times per second, which told him that it was a rapidly spinning pulsar. These so-called millisecond pulsars are neutron stars that spin hundreds of times per second, faster than a kitchen blender. Normally, the spin rate of neutron stars slows down as they age, but much like we can pull a string to “spin up“ a top, gas spiraling onto a neutron star from its companion can maintain or even increase its fast spin.
In the case of SWIFT J1756.9-2508, Markwardt detected subtle modulations in the X-ray timing data that revealed a low-mass companion tugging the pulsar toward and away from Earth. His calculations show that the companion has a minimum mass about 7 times that of Jupiter. Because we don’t know the orbital inclination of the system, the companion’s actual mass is unknown, but it is extremely unlikely to exceed 30 Jupiters.
MIT astronomers led by Deepto Chakrabarty also observed the system with RXTE, before it faded to invisibility on June 21. Chakrabarty’s group reached identical conclusions, and the two teams have coauthored a paper that has been accepted for publication in the Astrophysical Journal Letters.
The system is only the eighth millisecond pulsar that is observed to be accreting mass from a companion. Only one other such system has a pulsar companion with such a low mass. The companion in this system, XTE J1807-294, also has a minimum mass of about 7 Jupiters. “Given that we don’t know the exact mass of either companion, ours could be the smallest,“ says Krimm.
Evolution models by Christopher Deloye of Northwestern University suggest that the low-mass companion is helium dominated. “Despite its extremely low mass, the companion isn’t considered a planet because of its formation,“ says Deloye. “It’s essentially a white dwarf that has been whittled down to a planetary mass.“
After billions of years, little remains of the companion star, and it remains unclear whether it will survive. “It’s been taking a beating, but that’s part of nature,“ adds Krimm.
With an estimated distance of roughly 25,000 light-years, the system is normally too faint to be detected at any wavelength, and is only visible during an outburst. SWIFT J1756.9 has never been seen to erupt until this June, so as Markwardt points out, “We don’t know how long it will slumber before it wakes up again.“

Researchers at Deakin University have found that diesel exhaust is far more damaging to our health than exhaust from biodiesel, the plant-based fuel.
Associate Professor Leigh Ackland, Associate Head of Deakin’s School of Life and Environmental Sciences, led a team of researchers who compared the effects of diesel exhaust and biodiesel exhaust on human airway cells. They found that diesel exhaust damaged and killed the cells, while biodiesel exhaust had little effect, Science Daily reported.
“Australia’s escalating need for fuel is posing a major health problem,“ Associate Professor Ackland said.
“The fumes from burning fuels, including diesel, contributes to pollution and can cause heart disease, bronchitis and asthma. Efforts are underway to replace petrol and diesel with cleaner biofuels, such as biodiesel, but there is considerable resistance to this.
“This study provides clear evidence that diesel exhaust is more harmful to our health than biodiesel exhaust.“
As it is not possible to study in real time what happens in the real human airway, the researchers conducted their research on human airway cells grown in a culture. The cells were exposed to the particulate matter emitted in diesel and biodiesel exhaust fumes.
“Particulate matter is the burnt material, including carbon particles, emitted into the air. This particulate matter is part of biodiesel and diesel fumes but the particles produced from biodiesel were much less damaging to the cells than particles produced from diesel,“ Associate Professor Ackland explained.
“Our research found that the particulate matter from diesel exhaust stimulated a ’death pathway’ response that the body uses to dispose of damaged cells. This response caused the airway cells to fuse together and die. “We saw hardly any cell death after treatment with biodiesel particulates.“
Associate Professor Ackland said that the results of the study provide support for calls to move towards replacing petrol and diesel with cleaner biofuels.
“It is clear that breathing in diesel fumes is going to have a far more detrimental effect on our health than biodiesel. Given the level of cell death we have found, diesel exhaust could be the cause of respiratory disorders such as asthma and could even be implicated in cancer,“ she said.
The study has been published in the lastest edition of the international journal Immunology and Cell Biology.

Vital clues that might lead to an AIDS vaccine have been discovered by researchers studying the genetic code of HIV-2--the less virulent and less common form of the virus.
Although both forms of the virus infect humans, HIV-2 goes on to cause AIDS in only 20 per cent of infected people. In contrast, HIV-1, which has spread disastrously through sub-Saharan Africa, goes on to cause AIDS in 98 per cent of people who do not take anti-viral drugs, NewScientist.com reported.
A team from Oxford University and the UK Medical Research Council (MRC) unit in the Gambia set out to determine why the human immune system is better able to resist HIV-2, which is largely confined to West Africa. Their studies centered on a group of women infected with the virus for over a decade.
They discovered that a tiny part of one viral gene called gag makes HIV-2 vulnerable to attack from the human immune system. What’s more, this gene hardly ever mutates.
The gag gene, which codes for just 18 amino acids, provides a signal for white blood cells, called T-cells, to attack the virus and sweep it out of the blood stream before it can do further damage.
“Clearly there is something special about the gag region--and it looks like vaccine researchers should be focusing on it,“ says Aleksandra Leligdowicz who leads the MRC unit. The thinking is that a vaccine containing the right part of the gag gene could trigger the body’s immune response, making it better able to prevent HIV-2 infection developing into full blown AIDS.
Leligdowicz notes that the two per cent of people infected with HIV-1 who do not progress to AIDS show a strong T-cell response to the gag region as well.
Even more intriguing, most strains of HIV-1 also have a highly-conserved gag gene. The key to better vaccines could be finding just the right part of this region to include, she says.
The findings also indicate that a T-cell based or “cell mediated“ defense against HIV is enough to render HIV harmless. For over a decade researchers have argued whether or not an immune response that involved antibodies in addition to T-cells was also vital.
According to Leligdowicz, the latest results suggest it is possible to devise a vaccine to treat HIV, which although not preventing infection or eradicating the virus, will stop the wearing down of the immune system that leads to AIDS.
Virologist Robin Weiss who researches HIV vaccines at University College London says. “Ultimately, I think that a vaccine that actually prevents infection will need to make an anti-body response as well as cell-mediated one.
“But the idea of a therapeutic vaccine does have legs. Not only would it treat people, it might make them less able to infect other people, so you would get a double dividend. The study of HIV-2, although a less important pathogen, might well teach us some valuable lessons.“

The pigment melanin, which is responsible for skin and hair color in mammals, is produced in specialized cells called melanocytes and then distributed to other cells. But not every cell in the complex layers of skin becomes pigmented. The question of how melanin is delivered to appropriate locations may have been answered by a study from researchers at the Massachusetts General Hospital (MGH) Cutaneous Biology Research Center (CBRC).
“Pigment recipient cells essentially tell melanocytes where to deposit melanin, and the pattern of those recipients determines pigment patterns,“ says Janice Brissette, PhD, who led the study. “Recipient cells act like the outlines in a child’s coloring book; as recipient cells develop, they form a ’picture’ that is initially colorless but is then ’colored in’ by the melanocytes.“
In humans, melanin is deposited in both the skin and the hair; but in some other mammals such as mice, melanin is primarily deposited in the coat, leaving the skin beneath the coat unpigmented. Melanocytes deposit melanin via cellular extensions called dendrites that reach out to other cells in the epidermis (the outer layer of skin) or the hair follicles. But the mechanism determining whether melanin is delivered to a particular cell has been unknown, Science Daily said.
The MGH-CBRC researchers theorized that a mouse gene known as Foxn1 might play a role. Lack of Foxn1 is responsible for so-called ’nude mice,’ which have hair that is so brittle it breaks off, resulting in virtually total hairlessness, and other defects of the skin. A similar phenomenon exists in humans with inactivation of the corresponding gene.
When the researchers developed a strain of transgenic mice in which Foxn1 is misexpressed in cells that do not usually contain melanin, they found those normally colorless areas became pigmented. Examining the skin of the transgenic mice revealed that melanocytes were contacting and delivering melanin to the cells in which Foxn1 was abnormally activated. No pigment was observed in the corresponding tissues of normal mice. Examination of human skin samples showed that the human version of Foxn1 was also expressed in cells known to be pigment recipients. Further experiments revealed that Foxn1 signals melanocytes through a protein called Fgf2, levels of which rise as Foxn1 expression increases.
“Foxn1 makes epithelial cells into pigment recipients, which attract melanocytes and stimulate pigment transfer, engineering their own pigmentation,“ says Brissette, an associate professor of Dermatology at Harvard Medical School. She and her colleagues note that the Foxn1/Fgf2 pathway probably has additional functions in the skin and that it is probably not the only pathway responsible for the targeting of pigment.
“We know that Foxn1 and Fgf2 act in concert with other factors and function within a larger network of genes. Our next step will be to identify other genes that can confer the pigment recipient phenotype or control the targeting of pigment,“ Brissette adds. Her research may eventually be relevant to disorders such as vitiligo--in which pigment disappears from patches of skin--age spots, the greying of hair and even the deadly melanocyte-based skin cancer melanoma.

Low-fat, plant-based diets may help prevent or slow the progression of prostate cancer, according to a new research review.
A number of studies, though not all, have suggested that eating plenty of fruits and vegetables may help ward off prostate cancer, while “Western“-style diets heavy in animal fat and dairy products may increase a man’s risk of developing the disease, Reuters said.
In the current study, researchers reviewed 25 previously published studies that examined the effects of plant-based diets on prostate cancer development or progression.
Overall, the evidence suggests that diets high in fiber, fruits and vegetables, and low in meat and dairy, can help battle the disease, they report in the journal Nutrition Reviews.
For example, several studies of men with prostate cancer have linked high saturated fat intake to faster disease progression and a higher risk of death. Saturated fat is found mainly in animal products. In contrast, some small trials have found that a high-fiber, low-fat vegetarian diet may slow the growth and spread of early-stage prostate tumors. Some other studies have suggested that components of plant-based foods--like certain antioxidants or soy isoflavones--might be beneficial.
“For men diagnosed with prostate cancer, the key to improving the odds of survival is avoiding high-fat fare and instead choosing fruits, vegetables, beans and other cancer-fighting vegetarian foods,“ lead study author Dr. Susan Berkow said in a statement.
Berkow is with George Mason University in Alexandria, Virginia, and serves as a consultant to Physicians Committee for Responsible Medicine, a group that advocates vegetarian and vegan diets.
Berkow and her colleagues speculate that the fiber and other nutrients found in plant-based diets may affect prostate cancer by altering levels of certain hormones that can feed tumor development, including testosterone and insulin.
The balance of fats in a man’s diet may also be key, the researchers point out.

Researchers at Emory University in Atlanta are planning to screen healthy patients for biological and genetic clues to future illnesses.
Emory doctors believe focusing on so-called biomarkers can foreshadow diseases years before they occur, pointing patients to drugs and lifestyle changes that could help them stay healthy, UPI said.
If successful, the $50 million research initiative could result in fundamental changes to the American health care system, the researchers said.
Initiative leader Dr. Kenneth Brigham says until now research has always focused on what went wrong, not what went right.
“We don’t do much health care,“ Brigham says. “We do disease care.“
Emory doctors believe the new strategy can cut health care spending dramatically by allowing patients to be treated long before they need costly, crisis intervention.
It does, however, present new ethical questions such as what information should be disclosed to patients and whether insurance companies and employers will gain access to it.