Sodas, processed foods can accelerate signs of aging

Washington, Apr 27 (ANI): High levels of phosphate in sodas and processed foods can accelerate the aging process in mice and contribute to age-associated complications such as chronic kidney disease, claims a new study.

The study has been published in the FASEB Journal.

“Humans need a healthy diet and keeping the balance of phosphate in the diet may be important for a healthy life and longevity,” said M. Shawkat Razzaque, M.D., Ph.D., from the Department of Medicine, Infection and Immunity at the Harvard School of Dental Medicine. “Avoid phosphate toxicity and enjoy a healthy life.”

To reach the conclusion, Razzaque and colleague examined the effects of high phosphate levels in three groups of mice. The first group of mice was missing a gene (klotho), which when absent, causes mice to have toxic levels of phosphate in their bodies. These mice lived 8 to 15 weeks.

The second group of mice was missing the klotho gene and a second gene (NaPi2a), which when absent at the same time, substantially lowered the amount of phosphate in their bodies. These mice lived to 20 weeks. The third group of mice was like the second group (missing both the klotho and NaPi2a genes), except they were fed a high-phosphate diet. All of these mice died by 15 weeks, like those in the first group. This suggests that phosphate has toxic effects in mice, and may have a similar effect in other mammals, including humans.

“Soda is the caffeine delivery vehicle of choice for millions of people worldwide, but comes with phosphorous as a passenger” said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. “This research suggests that our phosphorous balance influences the aging process, so don”t tip it.” (ANI)

New discovery may lead to improved therapies for lung disease

Washington, Sept 16 (ANI): Researchers at The University of Texas Health Science Centre at Houston have discovered a protein that appears to play a crucial role in development of chronic obstructive pulmonary disease (COPD).

The protein called osteopontin (OPN) could lead to a novel approach to the treatment of a devastating lung disease.

The research conducted on mice showed that genetically removing osteopontin could prevent COPD.

The mice without the protein had less inflammation and lung disease.

“The lack of osteopontin in the mice prevented the COPD features,” said Daniel Schneider, the study’s lead author and an M.D./Ph.D. candidate at the UT Health Science Center at Houston.

To understand the applicability of their findings to humans, the researchers analyzed the airways of people with COPD and found elevated levels of the protein.

“This is an important crossover study,” said Dr Michael Blackburn, the study’s senior author and professor in the Department of Biochemistry and Molecular Biology at The University of Texas Medical School at Houston.

“Because we can show osteopontin is elevated in people with COPD, this suggests that osteopontin could serve as both an indicator of disease progression and a therapeutic target,” he added.

The findings appear online in The FASEB Journal. (ANI)

Here’s what ups amyloid beta production in Alzheimer’s patients’ brains

Washington, September 4 (ANI): A new class of medicines to effectively treat Alzheimer’s disease may soon be available, for an international research group has shed light on how a fragment of a protein increases the production of the amyloid beta protein in the brain.

The researchers say that knowing that the N60 fragment of the RanBP9 protein increases the production of the amyloid beta protein, which is present in excessive amounts in the brains of people with Alzheimer’s disease, gives scientists a more specific focus for developing new drugs.

Most experts believe that if the creation of amyloid beta protein can be halted or slowed, the devastating effects of Alzheimer’s disease may also be stopped or slowed too, according to background information in a research article published in the FASEB Journal.

David Kang, assistant professor of neurosciences at the University of California, San Diego, and one of the researchers involved in the work, said: “Our study suggests that targeting RanBP9 expression and/or N60 fragment generation may lead to novel strategies to combat this devastating disease.”

During the study, Kang and his colleagues examined extracts from brains with Alzheimer’s disease and age-matched healthy controls.

The researchers found that the N60 section of RanBP9 was increased in Alzheimer’s brain.

“Alzheimer’s might seem hopeless to some, but this research shows that we’re closer than ever to unraveling both the protein tangles and mysteries surrounding this devastating disease,” said Dr. Gerald Weissmann, the Editor-in-Chief of The FASEB Journal. (ANI)

Scientists imitate viruses to deliver therapeutic genes

Washington, September 1 (ANI): Australian scientists have developed a new gene therapy vector that uses the same machinery as viruses to transport their cargo into cells.

David Jans, from the Nuclear Signaling Laboratory at Monash University in Victoria, says that this achievement has raised the hope that one day therapeutic DNA will begin to be transferred to a cell’s nucleus far more efficiently than in the past, and thus there will be more effective treatments for several genetic disorders and some types of cancers.

“Through the use of proteins that mimic key functions of viruses for the packaging and transport of therapeutic DNA, we hope to improve the efficiency, and above all, the specificity of human gene therapy,” he said.

“Following the creation of efficient, specific and safe DNA delivery vectors, the challenges in human gene therapy will be able to move on from questions of delivery to actual clinical application,” he added.

A gene therapy vector is used to deliver a therapeutic gene or a portion of DNA into a cell nucleus similar to how a syringe is used to inject medicines.

To create the new gene therapy vector, Jans and his colleagues used pieces of different genes to create a protein called a “modular DNA carrier”, which can be produced by bacteria.

Writing about their work in The FASEB Journal, the researchers have revealed that this protein carries and delivers therapeutic DNA to a cell’s nucleus, where it reprograms a cell to function properly.

While experimenting in their laboratory, the research team combined these carrier proteins with therapeutic DNA, and attached them to cell membrane receptors and the nuclear import machinery of target cells.

In turn, according to the researchers, the packaged DNA moved into the cell through the cytoplasm and into the nucleus.

“Effective gene therapy is clearly the best way to treat heritable diseases. It’s also an approach to other diseases where the environment or infection messes up our genes.” said Dr. Gerald Weissmann, the Editor-in-Chief of The FASEB Journal.

“The Australians have worked out how viruses identify our nuclear ZIP-code, and have delivered therapeutic genes to the same address. This work opens up a new era of pharmaceutical development,” Dr. Weissmann added. (ANI)

High-fat diets ‘make us lazy, forgetful’

Washington, Aug 13 (ANI): Eating hotdogs and French fries might be a great treat, however, these high fat diets can significantly reduce our exercising ability and lead to short term memory loss, reveals a new study.

The research conducted using mouse model showed that in less than 10 days of eating a high-fat diet, rats had a decreased ability to exercise and experienced significant short-term memory loss.

“Western diets are typically high in fat and are associated with long-term complications, such as obesity, diabetes, and heart failure, yet the short-term consequences of such diets have been given relatively little attention,” said Andrew Murray, co-author of the study and currently at the University of Cambridge in the United Kingdom.

“We hope that the findings of our study will help people to think seriously about reducing the fat content of their daily food intake to the immediate benefit of their general health, well-being, and alertness,” he added.

Study leader Murray fed rats with low-fat diet (7.5 percent of calories as fat) and high-fat diet (55 percent of calories as fat).

He discovered that the muscles of the rats eating the high-fat diet for four days were less able to use oxygen to make the energy needed to exercise, causing their hearts to worker harder-and increase in size.

After nine days on a high-fat diet, the rats took longer to complete a maze and made more mistakes in the process than their low-fat-diet counterparts.

The researchers also studied the cellular causes of these problems, particularly in the mitochondria of muscle cells.

They found increased levels of a protein called uncoupling protein 3, which made them less efficient at using oxygen needed to make the energy required for running.

The new research is published online in The FASEB Journal. (ANI)

Biological ‘fountain of youth’ found in new world bat caves

Washington, July 1 (ANI): An Indian-origin researcher in Texas has announced a discovery that may lead to the single most important medical breakthrough in human history-significantly longer lifespans.

Writing about the finding in The FASEB Journal, VA Medical Center’s Professor Asish Chaudhuri says that proper protein folding over time in long-lived bats explains why they live significantly longer than other mammals of comparable size, such as mice.

“Ultimately we are trying to discover what underlying mechanisms allow for some animal species to live a very long time with the hope that we might be able to develop therapies that allow people to age more slowly,” said the senior researcher.

His team made this discovery by extracting proteins from the livers of two long-lived bat species-Tadarida brasiliensis and Myotis velifer-and young adult mice.

The researchers exposed the livers extracted to chemicals known to cause protein misfolding.

After examining the proteins, they found that the bat proteins exhibited less damage than those of the mice, indicating that bats have a mechanism for maintaining proper structure under extreme stress.

“Maybe Juan Ponce De Leon wasn’t too far off the mark when he searched Florida for the Fountain of Youth,” said Dr. Gerald Weissmann, Editor-in-Chief of The FASEB Journal.

“As it turns out, one of these bat species lives out its long life in Florida. Since bats are rodents with wings, this chemical clue as to why bats beat out mice in the aging game should point scientists to the source of this elusive fountain,” Dr. Weissmann added. (ANI)

Now, a one-two punch approach to KO HIV

Washington, May 29 (ANI): Making a major pharmaceutical breakthrough, scientists at St George’s, University of London have devised a one-two punch way to stop HIV.

In the study, the researchers have described a new protein that can kill the virus when used as a microbicide.

The researchers have also shown how the protein could be manufactured in quantities large enough to make it affordable for people in developing countries.

“We desperately need to control the spread of HIV, particularly in developing countries. A vaccine is still some way off, but microbicides could provide a more immediate solution, provided we can overcome major hurdles of high efficacy, low cost, and wide availability-all of which we address in this study,” said Julian Ma the senior researcher involved in the work.

The researchers have described how they combined two protein microbicides (b12 monoclonal antibody and cyanovirin-N) into a single “fusion” molecule and showed that this molecule is more active against HIV than either of its individual components.

They designed synthetic DNA for producing this molecule and introduced this DNA into plant cells.

Then they regenerated transgenic plants that produce the fusion molecule, and prepared the microbicide from a plant extract made by grinding the leaves.

“This study is nothing short of a breakthrough-not only does it yield a new drug to fight the spread of HIV, but it also shows us how we can produce it on the scale necessary to get it into the hands of those who need it most,” said Dr. Gerald Weissmann, Editor-in-Chief of The FASEB Journal.

He added: “Unlike their unregulated counterparts in the dietary supplement industry, these scientists are using the engines of nature to manufacture pharmaceuticals that must undergo extensive safety and efficacy testing long before the first gel or cream is administered.”

The study is published online in The FASEB Journal. (ANI)

Our ‘potheads’ make their own marijuana

Washington, Apr 21 (ANI): Our brain makes proteins that act directly on the marijuana receptors in the head, say researchers.

In the new study in FASEB Journal, researchers have discovered that the brain manufactures proteins that act like marijuana at specific receptors in the brain itself.

The discovery may lead to new marijuana-like drugs for managing pain, stimulating appetite, and preventing marijuana abuse.

“Ideally, this development will lead to drugs that bind to and activate the THC receptor, but are devoid of the side effects that limit the usefulness of marijuana,” said Lakshmi A. Devi of the Department of Pharmacology and Systems Therapeutics at Mount Sinai School of Medicine in New York and one of the senior researchers involved in the study.

“It would be helpful to have a drug that activated or blocked the THC receptor, and our findings raise the possibility that this will lead to effective drugs with fewer side effects,” she added.

Scientists made their discovery by first extracting several small proteins, called peptides, from the brains of mice and determining their amino acid sequence. The extracted proteins were then compared with another peptide previously known to bind to, but not activate, the receptor (THC) affected by marijuana. Out of the extracted proteins, several not only bound to the brain’s THC receptors, but activated them as well.

“The War on Drugs has hit very close to home,” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal.

“Last year, scientists found that our skin makes its own marijuana-like substance. Now, we see that our brain has been making proteins that act directly on the marijuana receptors in our head. The next step is for scientists to come up with new medicines that eliminate the nasty side of pot-a better joint, so to speak,” the expert added. (ANI)

You’re what your mum did not eat during pregnancy

Washington, Apr 14 (ANI): Researchers from University of Utah have found that lack of proper nutrition in the womb may cause permanent genetic changes in the offspring.

In the study conducted using rats, the researchers found that fetuses receiving poor nutrition in the womb become genetically primed to be born into an environment lacking proper nutrition. As a result, the rats were likely to grow to smaller sizes than their normal counterparts.

They were at higher risk for health problems throughout their lives, such as diabetes, growth retardation, cardiovascular disease, obesity, and neurodevelopmental delays.

“Our study emphasizes that maternal-fetal health influences multiple healthcare issues across generations,” said Robert Lane, professor of pediatric neonatology at the University of Utah, and one of the senior researchers involved in the study.

“To reduce adult diseases such as diabetes, obesity, and cardiovascular disease, we need to understand how the maternal-fetal environment influences the health of offspring,” he added.

During the study, the researchers included two groups of rats. The first group was normal. The second group had the delivery of nutrients from their mothers’ placentas restricted in a way that is equivalent to preeclampsia.

The rats were examined right after birth and again at 21 days (21 days is essentially a preadolescent rat) to measure the amount of a protein, called IGF-1, that promotes normal development and growth in rats and humans.

They found that the lack of nutrients caused the gene responsible for IGF-1 to significantly reduce the amount of IGF-1 produced in the body before and after birth.

The findings are published online in The FASEB Journal. (ANI)

You’re what your mum did not eat during pregnancy

Washington, Apr 14 (ANI): Researchers from University of Utah have found that lack of proper nutrition in the womb may cause permanent genetic changes in the offspring.

In the study conducted using rats, the researchers found that fetuses receiving poor nutrition in the womb become genetically primed to be born into an environment lacking proper nutrition. As a result, the rats were likely to grow to smaller sizes than their normal counterparts.

They were at higher risk for health problems throughout their lives, such as diabetes, growth retardation, cardiovascular disease, obesity, and neurodevelopmental delays.

“Our study emphasizes that maternal-fetal health influences multiple healthcare issues across generations,” said Robert Lane, professor of pediatric neonatology at the University of Utah, and one of the senior researchers involved in the study.

“To reduce adult diseases such as diabetes, obesity, and cardiovascular disease, we need to understand how the maternal-fetal environment influences the health of offspring,” he added.

During the study, the researchers included two groups of rats. The first group was normal. The second group had the delivery of nutrients from their mothers’ placentas restricted in a way that is equivalent to preeclampsia.

The rats were examined right after birth and again at 21 days (21 days is essentially a preadolescent rat) to measure the amount of a protein, called IGF-1, that promotes normal development and growth in rats and humans.

They found that the lack of nutrients caused the gene responsible for IGF-1 to significantly reduce the amount of IGF-1 produced in the body before and after birth.

The findings are published online in The FASEB Journal. (ANI)

Coming soon, a sureshot way to treat constipation

Washington, April 9 (ANI): Suffering from constipation? Well, help is on the way – a team of researchers has identified a potential drug target to make it a lot easier to go to the bathroom, especially when all other methods fail.

They have discovered a group of nerve ending receptors, which, when stimulated, causes the bowels to pass waste, and the specific receptor needed to activate bowel clearance.

Also, they tested chemicals that work with those receptors, providing a blueprint for the development of new laxatives.

“We hope that the receptor identified by our study would be exploited more in the design of drugs to treat constipation,” said Bindu Chandrasekharan, a researcher from Emory University who was involved in the study.

The study involved two groups of mice, focusing on a type of receptor also present on human nerves in the gut (a type of adenosine receptor).

The first group of mice had normal adenosine receptors on these nerves and normal bowel movements. The second group of mice completely lacked these adenosine receptors and showed familiar signs of constipation.

The researchers started with simple experiments such as comparing the wet weight, dry weight, and water content in the stools of both groups.

The mice were also made to drink a dye not absorbed by the body to see how it passed or did not pass.

In addition, the researchers used microscopic lasers to separate the nerve cells from the bowel to determine exactly where the receptors are located. Then they tested various chemicals that can activate or inhibit the nerve receptors.

Gerald Weissmann, M.D, Editor-in-Chief of The FASEB Journal, said: “Here’s why: First, we can look forward to a solution to what is sometimes a serious problem, especially infants and the elderly. Second, it’s the first definitive proof that these receptors, the adenosine receptors, control bowel function. This discovery promises to yield agents that will permit us to sit down and ease up in the middle of a busy day.”

The study has been published online in The FASEB Journal. (ANI)

Space experiment sheds new light on bone loss

Washington, March 31 (ANI): A space experiment conducted by Italian scientists has for the first time shown that a lack of resistance, that is gravity, activates bone-destroying cells.

An article on the study says that the finding attains significance as it may help better understand why bedridden patients and astronauts experience bone loss.

Published in The FASEB Journal, the article also says that the outcome provides an entirely new drug target for stopping the process.

“This study cuts straight to the bone in terms of why our skeletons deteriorate with disuse,” said Dr. Gerald Weissmann, Editor-in-Chief of the journal.

“As is the case with human intelligence, bone loss is an example of ‘use it or lose it’. This study from space has pinpointed the cellular culprits that destroy our bones when we don’t use them to support weight,” Weissmann added.

The researchers used two sets of bone-destroying cells, called “osteoclasts”, obtained from the bone marrow of mice femurs.

They launched one set into space via the European Space Agency’s 2007 FOTON-M3 mission, and kept the other set on Earth.

On the satellite, the cells were maintained in custom-designed bioreactors equipped with automatic nutrient providers.

At the same time, the other set of cells were kept in the same type of bioreactors on the Earth’s surface.

The experiment was stopped after twelve days, and the cells were examined.

The researchers found an increase in genes involved in osteoclast maturation and activity, as well as increased bone loss when compared to the cells on Earth.

“Space might be the final frontier, but we’ve got some serious hurdles to clear before we conquer microgravity, and bone loss is one of them,” Weissmann said.

“Even here on Earth, we all face bone loss. Osteoporosis inexorably hits men and women alike, and this European study points to one cause: lack of resistance,” Weissmann added. (ANI)

Scientists create ‘switch’ that turns stem cells into muscle

Washington, March 31 (ANI): American scientists have created a “switch” that allows mutations or light signals to be turned on in muscle stem cells to monitor muscle regeneration in a living mammal.

The research team, including 2007 Nobel Prize winner Mario R. Capecchi, say that their breakthrough may lead to a genetic switch, or drugs, that allows people to grow new muscle cells to replace those that are damaged, worn out, or non-functional.

The researchers also say that their work provides a new tool for studying muscle cancers, which are very difficult to treat.

“We hope that the genetically-engineered mouse models we developed will help scientists and clinicians better understand how to make muscle stem cells regenerate muscle tissue,” said Dr. Charles Keller, assistant professor at the University of Texas Health Science Center and a senior researcher involved in the work.

“For our own work on childhood muscle cancers, we also hope to understand how tumours start and progress, and to develop therapies that are less toxic than chemotherapy,” he added.

The researchers have revealed that they made this advance by breeding mice with a specific gene called “Cre”, which, when activated, can trigger mutations in muscle stem cells.

They point out that this Cre trigger is restricted to muscle stem cells and requires a special drug for it to be activated.

During the study, the researchers used fluorescent techniques that allowed them to visualize stem cells and their derivatives, in order to pinpoint exactly where muscle tissue was being made.

The team say that, in one part of the study, they were also able to activate tumour-causing mutations in muscle stem cells, providing valuable insights into the origins of muscle tumours, which have been previously elusive.

A report on the groundbreaking work has been published online in The FASEB Journal.

“This is basic science at its best. This study in mice has not only shown us how stem cells turn into muscle in the living body, but brought us closer to the day when we can use stem cells to repair wounded flesh or a maimed physique,” said Dr. Gerald Weissmann, Editor-in-Chief of the journal. (ANI)

Blind mole rat may serve as ‘living tumour’ in cancer research

Washington, March 5 (ANI): Studies on how blind mole rats survive very low oxygen environments can help win fight against cancer, say researchers.

American and Israeli scientists from the Universities of Illinois and Haifa have found that cellular mechanisms used by the blind mole rat to survive the very low oxygen environment of its subterranean niche are the same as those that tumours use to thrive deep in tissues.

During the study, the researchers conducted experiments in multiple groups of “dirty” mole rats and “regular” rats.

For each type of animal, a control group was exposed to normal levels of oxygen, while the experimental groups were exposed to oxygen levels ranging from 3 to 10 percent.

The researchers said that in the regular rats exposed to low levels of oxygen, the gene that becomes active to protect their bodies from low oxygen (BNIP3) was shown to be active in heart and skeletal muscles.

However, in the mole rats, it was discovered that their version of the BNIP3 gene was much more effective at helping them tolerate low levels of oxygen than the version of the gene in “regular” rats.

The researchers say that their findings suggest that the blind mole rat can serve a “living tumour” in cancer research.

Otherwise, they add, the unique gene in the blind mole rat may become a prime target for new anti-cancer drugs that can “suffocate” tumours.

A research article describing this study has been published in the FASEB Journal. (ANI)

Blind mole rat may serve as ‘living tumour’ in cancer research

Washington, March 5 (ANI): Studies on how blind mole rats survive very low oxygen environments can help win fight against cancer, say researchers.

American and Israeli scientists from the Universities of Illinois and Haifa have found that cellular mechanisms used by the blind mole rat to survive the very low oxygen environment of its subterranean niche are the same as those that tumours use to thrive deep in tissues.

During the study, the researchers conducted experiments in multiple groups of “dirty” mole rats and “regular” rats.

For each type of animal, a control group was exposed to normal levels of oxygen, while the experimental groups were exposed to oxygen levels ranging from 3 to 10 percent.

The researchers said that in the regular rats exposed to low levels of oxygen, the gene that becomes active to protect their bodies from low oxygen (BNIP3) was shown to be active in heart and skeletal muscles.

However, in the mole rats, it was discovered that their version of the BNIP3 gene was much more effective at helping them tolerate low levels of oxygen than the version of the gene in “regular” rats.

The researchers say that their findings suggest that the blind mole rat can serve a “living tumour” in cancer research.

Otherwise, they add, the unique gene in the blind mole rat may become a prime target for new anti-cancer drugs that can “suffocate” tumours.

A research article describing this study has been published in the FASEB Journal. (ANI)

Breakthrough technique may help generate solid organs from stem cells

Washington, Mar 3 (ANI): Making a significant advance in the field of tissue engineering, scientists have developed a new technique that could help generate solid organs from stem cells in the absence of a reliable supply of blood to the interior of the developing structure.

Researchers at the Stanford University School of Medicine said that stem cells could thrive in segments of well-vascularized tissue temporarily removed from laboratory animals

And once the cells have nestled into the tissue’s nooks and crannies, it is possible to seamlessly reconnect the so-called “bioscaffold” to the animal’s circulatory system.

“Efforts to use tissue engineering to generate whole organs have largely failed primarily due to the lack of available blood vessels. Now we’ve essentially hijacked an existing structure to overcome this problem,” said Dr. Geoffrey Gurtner, associate professor of surgery.

The researchers said that they could do so by keeping the tissue adequately supplied with oxygen and nutrients while outside of the body.

The researchers speculated that the stem cells in the tissue could soon be induced to become an internal, living factory of healthy, specialized cells churning out proteins missing in people with conditions like hemophilia or diabetes.

In the long run, they hope to encourage the cells to become entire transplantable organs, such as livers or pancreases.

The technique also eliminates the chance of rejection or complications caused by the use of artificial or donor-scaffolding materials by utilizing the animal’s own tissue.

“Eventually science will find a way to fabricate an organ in all its complexity. But in the short term we need to find more options for patients who are dying while waiting for transplants,” said Gurtner.

The study features in the March issue of the FASEB Journal. (ANI)

Wisdom has nothing to do with going grey

Washington, February 24 (ANI): Contrary to the age-old belief that grey hair is a sign of wisdom, a team of European scientists have shown that going grey is caused by a massive build up of hydrogen peroxide due to wear and tear of our hair follicles.

Publishing their findings online in The FASEB Journal, the researchers said that the peroxide winds up blocking the normal synthesis of melanin, our hair’s natural pigment.

“Not only blondes change their hair colour with hydrogen peroxide. All of our hair cells make a tiny bit of hydrogen peroxide, but as we get older, this little bit becomes a lot. We bleach our hair pigment from within, and our hair turns grey and then white. This research, however, is an important first step to get at the root of the problem, so to speak,” said Dr. Gerald Weissmann, Editor-in-Chief of The FASEB Journal.

The researchers have revealed that they examined cell cultures of human hair follicles, and found that the build up of hydrogen peroxide was caused by a reduction of an enzyme that breaks up hydrogen peroxide into water and oxygen (catalase).

They also found that hair follicles could not repair the damage caused by the hydrogen peroxide because of low levels of enzymes that normally serve this function-MSR A and B.

The researchers said that high levels of hydrogen peroxide and low levels of MSR A and B disrupt the formation of an enzyme called tyrosinase, which leads to the production of melanin in hair follicles.

Melanin is the pigment responsible for hair colour, skin colour, and eye colour.

The researchers speculate that a similar breakdown in the skin could be the root cause of vitiligo.

“As any blue-haired lady will attest, sometimes hair dyes don’t quite work as anticipated. This study is a prime example of how basic research in biology can benefit us in ways never imagined,” Weissmann added. (ANI)

Gazing at belly buttons can land you your ideal love mate

Washington, Jan 31 (ANI): It has often been cited as a textbook example of a useless body part, but if a scientist is to be believed, belly button beauty may play a vital role in finding potential mates.

Aki Sinkkonen of the University of Helsinki, Finland says: “I was younger than nowadays, and some of my friends were discussing how some women have a beautiful umbilicus or navel.

“I was thinking, ‘How is this possible? If this is scar tissue, how is it possible that it can be beautiful?”

Sinkkonen, who published his idea recently in the FASEB Journal, told Discovery News there is plenty of evidence that there is more to the “useless” body part than that.

For instance, in many mammals, the navel forms a tiny, asymmetrical scar.

However, in humans, it is a visible and significant mark. Many cultures draw attention to it in art, Sinkkonen noted, and some wealthy people pay plenty to have their navel’s appearance enhanced.

To reach his conclusion, Sinkkonen pointed out a research by Charles Puckett and colleagues of the University of Misouri, which quizzed people to choose from a number of navels the one that was most attractive.

The subjects agreed: the best-looking navels were vertically oriented with a T-shape.

Those with particularly large belly buttons, or with any sort of protrusions — sorry, outies — or distortions, received lower scores. (ANI)